Investigação da participação de citocinas inflamatórias na medula espinhal de ratos na dor pós-incisional
Autor(a) principal: | |
---|---|
Data de Publicação: | 2012 |
Tipo de documento: | Dissertação |
Idioma: | por |
Título da fonte: | Biblioteca Digital de Teses e Dissertações da UFRRJ |
Texto Completo: | https://rima.ufrrj.br/jspui/handle/20.500.14407/14929 |
Resumo: | As diversas modalidades de dor são geradas e mantidas por diferentes mecanismos fisiopatológicos, devendo ser estudadas independentemente. A dor pós-operatória é uma forma comum e única de dor aguda e apesar dos avanços em seu estudo, permanece subtratada. Por causa da persistência da dor mesmo após o uso de medicamentos antiinflamatórios e opioides, postulamos que as citocinas possam desempenhar papel chave na dor pós-cirúrgica. Por meio de dados obtidos de testes nociceptivos, analisamos a concentração de citocinas inflamatórias liberadas pelo segmento lombar da medula espinhal de ratos submetidos ao modelo de dor pós-operatória. No teste de von Frey e no teste de Hargreaves, utilizados para avaliar a hiperalgesia mecânica e térmica, respectivamente, os animais tiveram redução dos limiares de retirada 1 hora após a incisão plantar que pode observada até as 72 horas após a cirurgia, quando comparados com animais sem incisão. Com base nesses resultados, foram feitas análises da liberação das citocinas pró-inflamatórias IL- 1β, IL-6 e TNF-α e das citocinas anti-inflamatórias IL-10 e IL-4 liberadas pela região lombar da medula espinhal pelo método de quimiluminescência às 2, 4, 6, 8, 12, 24, 48 e 72 horas após a incisão plantar. Através da técnica de qRT-PCR, as expressões gênicas de IL-1β, TNF- α e GFAP também foram avaliadas nos tempos de 2, 6, 48 e 72 horas após a incisão. Não houve alteração da liberação de IL-1β, IL-6, TNF-α e IL-4. Ocorreu diminuição significativa da liberação de IL-10 48 horas após a incisão quando comparado aos animais não incisados. Não houve alteração da expressão gênica de IL-1β, no entanto foi observado um aumento da expressão de TNF-α e GFAP 6 horas após a incisão quando comparados com animais não submetidos à incisão plantar. A incisão plantar não parece alterar a liberação das citocinas IL-1β, IL-6, TNF-α e IL-4. A manutenção da dor pós-operatória não está associada a uma queda sustentada dos níveis de IL-10. O aumento da expressão de RNAm de TNF-α condiz com o aumento da expressão de RNAm de GFAP e indica possível papel dos astrócitos na liberação da citocina. Porém, a manutenção da dor pós-operatória não está associada a um aumento constante da expressão gênica de TNF-α. O papel da liberação desta citocina na medula espinal no modelo de dor pós-operatória, assim como a confirmação da participação dos astrócitos necessitam ser investigados. |
id |
UFRRJ-1_ca84268bc9c91f6f9e807e67d2e97a17 |
---|---|
oai_identifier_str |
oai:rima.ufrrj.br:20.500.14407/14929 |
network_acronym_str |
UFRRJ-1 |
network_name_str |
Repositório Institucional da UFRRJ |
repository_id_str |
|
spelling |
Castro, Ligia Lins deMedeiros, Magda Alves de036592487-38http://lattes.cnpq.br/6392136073564306Otero, Rosalia MendezVanderlinde, Frederico Argolo116286767-10http://lattes.cnpq.br/68148688998835582023-12-22T03:08:29Z2023-12-22T03:08:29Z2012-07-05CASTRO, Ligia Lins de. Investigação da participação de citocinas inflamatórias na medula espinhal de ratos na dor pós-incisional. 2012. 42 f. Dissertação (Mestrado Multicêntrico em Ciências Fisiológicas) - Instituto de Ciências Biológicas e da Saúde, Universidade Federal Rural do Rio de Janeiro, Seropédica - RJ, 2012.https://rima.ufrrj.br/jspui/handle/20.500.14407/14929As diversas modalidades de dor são geradas e mantidas por diferentes mecanismos fisiopatológicos, devendo ser estudadas independentemente. A dor pós-operatória é uma forma comum e única de dor aguda e apesar dos avanços em seu estudo, permanece subtratada. Por causa da persistência da dor mesmo após o uso de medicamentos antiinflamatórios e opioides, postulamos que as citocinas possam desempenhar papel chave na dor pós-cirúrgica. Por meio de dados obtidos de testes nociceptivos, analisamos a concentração de citocinas inflamatórias liberadas pelo segmento lombar da medula espinhal de ratos submetidos ao modelo de dor pós-operatória. No teste de von Frey e no teste de Hargreaves, utilizados para avaliar a hiperalgesia mecânica e térmica, respectivamente, os animais tiveram redução dos limiares de retirada 1 hora após a incisão plantar que pode observada até as 72 horas após a cirurgia, quando comparados com animais sem incisão. Com base nesses resultados, foram feitas análises da liberação das citocinas pró-inflamatórias IL- 1β, IL-6 e TNF-α e das citocinas anti-inflamatórias IL-10 e IL-4 liberadas pela região lombar da medula espinhal pelo método de quimiluminescência às 2, 4, 6, 8, 12, 24, 48 e 72 horas após a incisão plantar. Através da técnica de qRT-PCR, as expressões gênicas de IL-1β, TNF- α e GFAP também foram avaliadas nos tempos de 2, 6, 48 e 72 horas após a incisão. Não houve alteração da liberação de IL-1β, IL-6, TNF-α e IL-4. Ocorreu diminuição significativa da liberação de IL-10 48 horas após a incisão quando comparado aos animais não incisados. Não houve alteração da expressão gênica de IL-1β, no entanto foi observado um aumento da expressão de TNF-α e GFAP 6 horas após a incisão quando comparados com animais não submetidos à incisão plantar. A incisão plantar não parece alterar a liberação das citocinas IL-1β, IL-6, TNF-α e IL-4. A manutenção da dor pós-operatória não está associada a uma queda sustentada dos níveis de IL-10. O aumento da expressão de RNAm de TNF-α condiz com o aumento da expressão de RNAm de GFAP e indica possível papel dos astrócitos na liberação da citocina. Porém, a manutenção da dor pós-operatória não está associada a um aumento constante da expressão gênica de TNF-α. O papel da liberação desta citocina na medula espinal no modelo de dor pós-operatória, assim como a confirmação da participação dos astrócitos necessitam ser investigados.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior, CAPES, Brasil.The several types of pain are generated and maintained by different pathophysiological mechanisms, and should be studied independently. The postoperative pain is a commom and single form of acute pain and despite advances in their study, remains undertreated. Because of persistent pain, even after the use of anti-inflammatory drugs and opiods, we postulated that cytokines may play a key role in post-surgical pain. By means of the data obtained from nociceptive tests, we analyzed the concentration of inflammatory cytokines released by the lumbar segment of spinal cord of rats submitted to the model of postoperative pain. In the von Frey test and Hargreaves test, used to evaluate the mechanical and thermal hyperalgesia, respectively, the animals had a reduction of paw withdrawal thresholds at 1 hour after plantar incision that can be observed until 72 hour after the surgery when compared to animals without incision. Based on these results, the releasing of proinflamatory cytokines IL-1β, IL-6 e TNF-α and anti- inflammatory cytokines IL-10 e IL-4 released by the lumbar spinal cord were analyzed by the chemiluminescence method at 2, 4, 6, 8, 12, 24,48 and 72 hours after the plantar incision. Using the qPCR-RT technique, the gene expression of IL-1β, TNF-α and GFAP were also evaluated at 2, 6, 48 and 72 hours following incision. There was a significant decrease in the release of IL-10 48 hours after the incision when compared to not incised animals. There was no change in the gene expression of IL-1β, however, there was increased in the expression of TNF-α and GFAP 6 hours after the incision when compared to animals not submitted to plantar incision. The plantar incision does not alter the release of cytokines IL-1β, IL-6, TNF-α and IL-4. The maintenance of postoperative pain is not associated with sustained decrease in levels of IL-10. The increase of the expression of TNF-α mRNA is consistent to the increase of the expression of GFAP mRNA and indicates a possible role of astrocytes in the release of cytokines. However, the maintenance of postoperative pain is not associated with constant increase of gene expression of TNF-α. The role of spinal cord release of cytokine in model of postoperative, as well as confirmation of contribution of astrocytes needs investigation.application/pdfporUniversidade Federal Rural do Rio de JaneiroPrograma Multicêntrico de Pós-Graduação em Ciências FisiológicasUFRRJBrasilInstituto de Ciências Biológicas e da Saúdedor pós-operatórianocicepçãocitocinaspostoperative painnociceptioncytokinesFisiologiaInvestigação da participação de citocinas inflamatórias na medula espinhal de ratos na dor pós-incisionalInvestigation of the involvement of inflammatory cytokines in rat spinal cord in incisional paininfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisALKAITIS, M.S.; SOLORZANO, C.; LANDRY, R. P.; PIOMELLI, D.; DELEO, J. A.; ROMERO-SANDOVAL, E.A. Evidence for a role of endocannabinoids, astrocytes and p38 phosphorylation in the resolution of postoperative pain. PLoS One, v. 5, p. 10891, 2010. AWATSUJI, H.; FURUKAWA, Y.; HIROTA, M.; MURAKAMI, Y.; NII, S. M.; FURUKAWA, S.; HAYASHI, K. Interleukin-4 and -5 as modulators of nerve growth factor synthesis/secretion in astrocytes. Journal of Neuroscience Research, v. 34, p. 539- 545, 1993. BEDBROOK, G.M. Injuries of the Thoracolumbar Spine with Neurological Symptoms, em: Vinken, P. J.; Bruyn, G. W. Handbook of Clinical Neurology, Amsterdam: North-Holland, 1976. p. 437 a 466. BISHOP, G.H.; LANDAU, W.M.; JONES, M.H. Evidence for a double peripheral pathway for pain. Science, v. 128, p. 712-714, 1958. BRENNAN, T.J.; VANDERMEULEN, E.P.; GEBHART, G.F. Characterization of a rat model of incisional pain. Pain, v. 64, p. 493-501, 1996. BRENNAN, T.J.; ZAHN, P.K.; POGATZKI, E.M. Mechanisms of incisional pain. Anesthesiology Clinics of North America, v. 23, p. 1-20, 2005. BRENNER, G. J.; JI, R.R.; SHAFFER, S.; WOOLF, C.J. Peripheral noxious stimulation induces phosphorylation of the NMDA receptor NR1 subunit at the PKCdependent site, serine-896, in spinal cord dorsal horn neurons. European Journal of Neuroscience, v. 20, p. 375-384, 2004. CAMPBELL, J.N.; RAJA, S.N.; COHEN, R.H. Peripheral Neural Mechanisms of Nociception, em: Wall, P.D.; Melzack, R. Textbook of Pain, Edimburgo: Churchill Livingstone, 1989. p. 22 a 45. CARSWELL, E.A.; OLD, L.J.; KASSEL, R.L. An endotoxin-induced serum factor that causes necrosis of tumors. Procedings of the National Academy of Sciences of the United States of America, v. 72, p. 3666-3670, 1975. CHAO, C.C.; MOLITOR, T.W.; HU, S. Neuroprotective role of IL-4 against activated microglia. Journal of Immunology, v. 151, p. 1473-1481, 1993. CHAORAN, W.; BOUSTANY, L.; LIANG, H.; BRENNAN, T.J. Nerve Growth Factor Expression after Plantar Incision in the Rat. Anesthesiology, v. 107, p. 128–135, 2007. CHEN, L.; ZHANG, J.; LI, F.; QIU, Y.; WANG, L.; LI, Y. H.; SHI, J.; PAN, H. L.; LI, M. Endogenous anandamide and cannabinoid receptor-2 contribute to electroacupuncture analgesia in rats. Journal of Pain, v. 10, p. 732-739, 2009. CSÓKA, B.; NÉMETH, Z.H.; VIRÁG, L.; GERGELY, P.; LEIBOVICH, S.J.; PACHER, P.; SUN, C.X.; BLACKBURN, M.R.; VIZI, E.S.; DEITCH, E.A.; HASKÓ, G. A2A adenosine receptors and C/EBPbeta are crucially required for IL-10 production by macrophages exposed to Escherichia coli. Blood, v. 110, p. 2685-2695, 2007. 35 CUNHA, F.Q.; POOLE, S.; LORENZETTI, B.B.; FERREIRA, S.H. The pivotal role of tumour necrosis factor alpha in the development of inflammatory hyperalgesia. British Journal of Pharmacology, v. 107, p. 660–664, 1992. CUNHA, F.Q.; POOLE, S.; LORENZETTI, B.B.; VEIGA, F.H.; FERREIRA, S.H. Cytokine- mediated inflammatory hyperalgesia limited by interleukin-4. British Journal of Pharmacology, v. 126, p. 45–50, 1999. CUNHA, J.M; CUNHA, F.Q; POOLE, S.; FERREIRA, S.H. Cytokinemediated inflammatory hyperalgesia limited by interleukin-1 receptor antagonist. British Journal of Pharmacology, v. 130, p. 1418-1824, 2000. CUNHA, T.M.; VERRI WA, J.R.; SILVA, J.S.; POOLE, S.; CUNHA, F. Q.; FERREIRA, S.H. A cascade of cytokines mediates mechanical inflammatory hypernociception in mice. Procedings of the National Academy of Sciences of the United States of America. v.102, p. 1755-1760, 2005. DA FONSECA PACHECO, D.; KLEIN, A.; DE CASTRO PEREZ, A.; DA FONSECA PACHECO, C.M.; DE FRANCISCHI, J.N., DUARTE, I.D. The mu-opioid receptor agonist morphine, but not agonists at delta- or kappa-opioid receptors, induces peripheral antinociception mediated by cannabinoid receptors. British Journal of Pharmacology, v. 154, p. 1143-1149, 2008. DINARELLO, C. A. Interleukin-1, interleukin-1 receptors and interleukin-1 receptor antagonist. International Rewiew Immunology, v. 16, p. 457-499, 1998. DINARELLO, C.A. Proinflammatory and anti-inflammatory cytokines as mediators in the pathogenesis of septic shock. Chest, v. 112, p. 321S-329S, 1997. D'MELLO, R.; DICKENSON, A.H. Spinal cord mechanisms of pain. British Journal of Anaesthesia, v. 101. p. 8-16, 2008. FENTON, M.J.; BURAS, J.A.; DONNELLY, R.P. IL-4 reciprocally regulates IL-1 and IL-1 receptor antagonist expression in human monocytes. Journal of Immunology, v. 149, p. 1283-1288, 1992. FERREIRA, S.H. Hiperalgesia inflamatórial, óxido nítrico y control periférico del dolor. RevLatino Americana de Dolor, v. 12, p. 6-17, 1995. FERREIRA, S.H.; LORENZETTI, B.B.; BRISTOW, A.F.; POOLE, S. Interleukin-1 beta as a potent hyperalgesic agent antagonized by a tripeptide analogue. Nature, v. 6184, p. 698-700, 1988. FU, D.; GUO, Q.; AI, Y.; CAI, H.; YAN, J.; DAÍ, R. Glial activation and segmental upregulation of interleukin-1beta (IL-1beta) in the rat spinal cord after surgical incision. Neurochemical Research, v. 31, p. 333-340, 2006. GAGLIESE, L.; MELZACK, R. Age differences in nociception and pain behaviours in the rat. Neuroscience and Biobehavioral Reviews, v. 24, p. 843-854, 2000. GUO, W.; ZOU, S.; GUAN, Y; IKEDA, T.; TAL, M.; DUBNER, R.; REN, K.; Tyrosine phosphorylation of the NR2B subunit of the NMDA receptor in the spinal cord during the development and maintenance of inflammatory hyperalgesia. Journal of Neuroscience, v. 22, p. 6208-6217, 2002. 36 HARGREAVES, K.; DUBNER, R.; BROWN, F., FLORES, C., JORIS, J. A new and sensitive method for measuring thermal nociception in cutaneous hyperalgesia. Pain, v. 32, p. 77-88, 1988. HASKO, G.; SZABO, C.; NEMETH, Z.H.; KVETAN, V.; PASTORES, S.M.; VIZI, E.S. Adenosine receptor agonists differentially regulate IL-10, TNF-alpha, and nitric oxide production in RAW 264.7 macrophages and in endotoxemic mice. Journal of Immunology, v. 157, p. 4634-4640. 1996. HUITINGA, I.; SCHMIDT, E.D.; VAN DER CAMMEN, M.J.; BINNEKADE, R.; TILDERS, F.J. Priming with inter- leukin-1beta suppresses experimental allergic encephalomyelitis in the Lewis rat. Journal of Neuroendocrinology, v. 12, p. 1186–1193, 2000. HUNT, S.P.; PINI, A.; EVAN, G. Induction of c-fos-like protein in spinal cord neurons following sensory stimulation. Nature, v. 328, p. 632-634, 1987. IBRAHIM, M.; PORRECA, F.; LAI, J.; ALBRECHT, P.J.; RICE, F.L.; KHODOROVA, A.; DAVAR, G.; MAKRIYANNIS, A.; VANDERAH, T.W.; MATA, H.P.; MALAN JR, F. CB2 cannabinoid receptor activation produces antinociception by stimulating peripheral release of endogenous opioids. PNAS, v. 102, p. 3093-3098, 2005. ISAACS, A. & LINDENMANN, J. Virus interference. I. The interferon. Journal of Interferon Research, v. 5, p. 429-438, 1957. ITO, N.; OBATA, H., SAITO, S. Spinal microglial expression and mechanical hypersensitivity in a postoperative pain model: comparison with a neuropathic pain model. Anesthesiology, v. 111, p. 640-648, 2009. JI, R.R.; SAMAD, T.A.; JIN, S.X. p38 MAPK activation by NGF in primary sensory neurons after inflammation increases TRPV1 levels and maintains heat hyperalgesia. Neuron, v. 36, p. 57-68, 2002. JI, R.R.; KOHNO, T.; MOORE, K.A. Central sensitization and LTP: do pain and memory share similar mechanisms? Trends of Neuroscience, v. 26, p. 696-705, 2003. JORDAN, M.; OTTERNESS, I.G.; NG, R.; GESSNER, A.; ROLLINGHOFF, M.; BEUSCHER, H.U. Neutralization of endogenous IL-6 suppresses induction of IL-1 receptor antagonist. Journal of Immunology, v. 154, p. 4081-4090, 1995. KANAAN, S.A.; POOLE, S.; SAADE, N.E.; JABBUR, S.; SAFIEHGARABEDIAN, B. Interleukin-10 reduces the endotoxin-induced hyperalgesia in mice. Journal of Neuroimmunology, v. 86, p. 142-150, 1998. KAWAKAMI, M.; CERAMI, A. Studies of endotoxin-induced decrease in lipoprotein lipase activity. The Journal of Experimental Medicine, v. 154, p. 6319, 1981. KAWASAKI, Y.; ZHANG, L.; CHENG, J.K.; JI, R.R. Cytokine mechanisms of central sensitization: distinct and overlapping role of interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha in regulating synaptic and neuronal activity in the superficial spinal cord. Journal of Neuroscience, v. 28, p. 5189–5194, 2008. 37 KAPLAN, M.D.; OLSCHOWKA, J.A.; O'BANION, M.K. Cyclooxygenase- 1 behaves as a delayed response gene in PC12 cells differentiated by nerve growth factor. The Journal of Biological Chemistry, v. 272, p. 534-537, 1997. KISSELEVA, T.; BHATTACHARYA, S.; BRAUNSTEIN, J.; SCHINDLER, C. W. Signaling through the JAK/STAT pathway, recent advances and future challenges. Gene, v. 285, p. 1-24, 2002. LAVICH, T.R.; CORDEIRO, R.S.B.; SILVA, P.M.R.; MARTINS, M.A. A novel hot-plate test sensitive to hyperalgesic stimuli and non-opioid analgesics. Brazilian Journal of Medical and Biological Research, v. 38, p. 445-451, 2005. LEDEBOER, A.; JEKICH B.M.; SLOANE, E.M.; MAHONEY, J.H.; LANGER, S.J.; MILIGAN, E.D. MARTIN, D.; MAIER, S.F.; JOHNSON, K.W.; LESLIE, A.; CHAVEZ, R.A.; WATKINGS, L.R. Intrathecal Interleukin-10 Gene Therapy Attenuates Paclitaxel Induced Mechanical Allodynia and Proinflammatory Cytokine Expression in Dorsal Root Ganglia in Rats. Brain, Behaviour, Immunity, v. 21, p. 686-698, 2007. LEE S.R.; GUO, S.Z.; SCANNEVIN, R.H.; MAGLIARO, B.C.; RHODES, K.J., WANG, X.; LO, E.H. Induction of matrix metalloproteinase, cytokines and chemokines in rat cortical astrocytes exposed to plasminogen activators. Neuroscience Letters, v. 417, p. 1-5, 2007. LEEM, J.W.; WILLIS, W.D.; CHUNG, J.M. Cutaneous sensory receptors in the rat foot. Journal of Neurophysiology, v. 69, p. 1684-1699, 1993. LI, C.; XU, J.; LIU, D.; ZHANG, J.; DAI, R. Brain derived neurotrophic factor (BDNF) contributes to the pain hypersensitivity following surgical incision in the rats. Molecular Pain, v. 4, p. 27, 2008. LI, X.; ANGST, M.S.; CLARK, J.D. Opioid-induced hyperalgesia and incisional pain. Anesthesia & Analgesia, v. 93, p. 204-209, 2001. LIANG, D.Y; SHI, X.; QIAO, X; ANGST, M.S.; YEOMANS C.D.; CLARK, J.D. Chronic morphine administration enhances nociceptive sensitivity and local cytokine production after incision. Molecular Pain, v. 4, p. 7, 2008. LOEWENSTEIN, W.R. Mechano-Electric Transduction in the Pacinian Corpuscle: Initiation of Sensory Impulses in Mechanoreceptors. Handbook of Sensory Physiology, Berlim: Springer-Verlag, 1971, p. 267 a 290. LORAM, L.C.; HARRISON, J.A.; SLOANE, E.M.; HUTCHINSON, M.R.; SHOLAR, P.; TAYLOR, F.R.; BERKELHAMMER, D.; COATS, B.D.; POOLE, S.; MILLIGAN, E.D.; MAIER, S.F.; RIEGER, J.; WATKINS, L.R. Enduring reversal of neuropathic pain by a single intrathecal injection of adenosine 2A receptor agonists: a novel therapy for neuropathic pain. Journal of Neuroscience, v. 29, p. 14015-14025, 2009. LORAM, L.C.; THEMISTOCLEOUS, A.C.; FICK, L.G.; KAMERMAN, P.R. The time course of inflammatory cytokine secretion in a rat model of postoperative pain does not coincide with the onset of mechanical hyperalgesia. Canadian Journal of Physiology and Pharmacology, v. 85, p. 613-620, 2007. LUCAS, S.M.; ROTHWELL, N.J.; GIBSON, R.M. The role of inflammation in CNS injury and disease. British Journal of Pharmacology, v. 147, p.S232-240, 2006. 38 MARCHAND, F.; PERRETI, M.; MC MAHON, S.B. Role of the immune system in chronic pain. Nature Reviews of Neuroscience, v. 6, p. 521-532, 2005. MILLER, A.J.; HOPKINS, S.J.; LUHESHI, G.N. Sites of action of IL-1 in the development of fever and cytokine responses to tissue inflammation in the rat. British Journal of Pharmacology, v. 120,p. 1274-1279, 1997. MÖLLER, K.A.; JOHANSSON, B.; BERGE, O.G. Assessing mechanical allodynia in the rat paw with a new electronic algometer. Journal of Neuroscience Methods, v. 84, p. 41-47, 1998. MOSSNER, R.; BECKMANN, I.; HALLERMANN, C.; NEUMANN, C.; REICH, K. Granulocyte colony-stimulating-factor-induced psoriasi form dermatitis resembles psoriasis with regard to abnormal cytokine expression and epidermal activation. Experimental Dermatology, v. 13, p. 340-346, 2004. NAKA, T.; NISHIMOTO, N.; KISHIMOTO, T. The paradigm of IL-6: from basic science to medicine. Arthritis Research, v. 4, p. S233-242, 2002. NICOLA, N. A.; NICHOLSON, S.E.; METCALF, D.; ZHANG, J.G.; BACA, M.; FARLEY, A.; WILLSON, T.A.; STARR, R.; ALEXANDER, W.; HILTON, D.J. Negative regulation of cytokine signaling by the SOCS proteins. Cold Spring Harbor Symposia Quantitative Biology, v. 64,p. 397-404, 1999. NODA, M.; NAKANISHI, H.; NABEKURA, J.; AKAIKE, N. AMPAkainate subtypes of glutamate receptor in rat cerebral microglia. Journal of Neuroscience, v. 20,p. 251-258, 2000. O’BANION, M.K. Cyclooxygenase-2: molecular biology, pharmacology, and neurobiology. Critical Reviews in Neurobiology, v. 13, p. 45-82, 1999. OBATA, H.; EISENACH, J.C.; HUSSAIN, H.; BYNUM, T.; VINCLER, M. Spinal Glial Activation Contributes to Postoperative Mechanical Hypersensitivity in the Rat. Journal of Pain, v. 7, p. 816-822, 2006. ONOE, Y.; MIYAURA, C.; KAMINAKAYASHIKI, T.; NAGAI, Y.; NOGUCHI, K.; CHEN, Q. R.; SEO, H.; OHTA, H. NOZAWA, S. KUDO, I.; SUDA, T. IL-13 and IL- 4 inhibit bone resorption by suppressing cyclooxygenase-2-dependent prostaglandin synthesis in osteoblasts. Journal of Immunology, v. 156, p. 758-764, 1996. PERKINS, M.N.; KELLY, D. Interleukin-1 beta induced-desArg9bradykininmediated thermal hyperalgesia in the rat. Neuropharmacology, vol. 5: p. 657-660, 1994. PIOTROWSKI, W.; FOREMAN, J.C. Some effects of calcitonin generelated peptide in human skin and on histamine release. British Journal of Dermatology, v. 114, p.37-46, 1986. POGATZKI, E.M.; GEBHART, G.F.; BRENNAN, T.J. Characterization of A- and C-fibers innervating the plantar rathindpaw one day after an incision. Journal of Neurophisiology, v. 87, p. 721-731, 2001. POGATZKI, E.M.; ZAHN, P.K.; BRENNAN, T.J. Postoperative pain-clinical implications of basic research. Best Practice & Research: Clinical Anaesthesiology, v. 21, p. 3-13, 2007. 39 POOLE, S.; CUNHA, F.Q.; SELKIRK, S.; LORENZETTI, B.B.; FERREIRA, S.H. Cytokine-mediated inflammatory hyperalgesia limited by interleukin-10. British Journal of Pharmacology, v. 115, p. 684-688, 1995. POOLE, S.; LORENZETTI, B.B.; CUNHA, J.M.; CUNHA, F.Q.; FERREIRA, S.H. Bradykinin B1 and B2 receptors, tumour necrosis factor alpha and inflammatory hyperalgesia. British Journal of Pharmacology, v. 126, p. 649-56, 1999. RANDIC, M. JIANG, M.C.; CERNE, R. Long-term potentiation and long term depression of primary afferent neurotransmission in the rat spinal cord. Journal of Neuroscience, v. 13, p. 5228-5241, 1993. REICHL, S.; AUGUSTIN, M.; ZAHN, P.K.; POGATZKI-ZAHN, E.M. Peripheral and spinal GABAergic regulation of incisional pain in rats. Pain, v. 153, p. 129-141, 2012. ROCHA, A.P.C.; KRAYCHETE, D.C.; LEMONICA, L.; CARVALHO, L.R.; BARROS, G.A.M.; GARCIA, J.B.S.; SAKATA, R.K. Dor: Aspectos Atuais da Sensibilização Periférica e Central. Revista Brasileira de Anestesiologia, v. 57, p. 94-105, 2007. ROMERO-SANDOVAL, A.; CHAI, N.; NUTILE-MCMENEMY, N.; DELEO, J.A. A comparison of spinal Iba1 and GFAP expression in rodent models of acute and chronic pain. Brain Research, v. 1219, p. 116-26, 2008. ROMERO-SANDOVAL, A.;EISENACH, J.C. Spinal cannabinoid receptor type 2 activation reduces hypersensitivity and spinal cord glial activation after paw incision. Anesthesiology, v. 106, p. 787-794, 2007. SANDKUHLER, J. Learning and memory in pain pathways. Pain, v. 88, p. 113-118, 2000. SCHAFERS, M.; SOMMER, C.; GEIS, C.; HAGENACKER, T.; VANDENABEELE, P.; SORKIN, L.S. Selective stimulation of either tumor necrosis factor receptor differentially induces pain behavior in vivo and ectopic activity in sensory neurons in vitro. Neuroscience, v. 157, p. 414-423, 2008. SCHAFERS, M.; SORKIN, L.S.; GEIS, C. SHUBAYEV. V.I. Spinal nerve ligation induces transient upregulation of tumor necrosis factor receptors 1 and 2 in injured and adjacent uninjured dorsal root ganglia in the rat. Neuroscience Letters, v. 347, p. 179-182, 2003. SHUAI, K. & LIU, B. Regulation of JAK–STAT signalling in the immune system. Nature Reviews Immunology, v. 3, p. 900-911, 2003. SPRANGER, M.; LINDHOLM, D.; BANDTLOW, C.; HEUMANN, R.; GNAHN, H. NTIER- NOE, M.; THOENEN, H. Regulation o f nerve growth factor (NGF) synthesis in the rat central nervous system: comparison between the effects o f interleukin- 1 and various growth factors in astrocyte cultures and in vivo. European Journal of Neuroscience, v. 2, p. 69-76, 1990. STARR, R. & HILTON, D.J. Negative regulation of the JAK/STAT pathway. Bioessays, v. 1, p. 47-52, 1999. 40 STELLWAGEN, D.; BEATTIE, E.C.; SEO, J.Y.; MALENKA, R.C. Differential regulation of AMPA receptor and GABA receptor trafficking by tumor necrosis factoralpha. Journal of Neuroscience, v. 25, p. 3219–3228, 2005. STRLE, K.; ZHOU, J.H.; SHEN, W.H.; BROUSSARD, S.R.; JOHNSON, R.W.; FREUND, G.G.; DANTZER, R.; KELLEY, K.W. Interleukin-10 in the brain. Critical Revewies in Immunology, v. 21, p. 427–449, 2001. SU, T.F.; ZHAO, Y.Q.; ZHANG, L.H.; PENG, M.; WU, C. H.; PEI, L.; TIAN, B., ZHANG, J.; SHI, J.; PAN, H.L.; LI, M. Electroacupuncture reduces the expression of proinflammatory cytokines in inflamed skin tissues through activation of cannabinoid CB2 receptors. European Journal of Pain, v. 16, p. 624-35, 2012. TILG, H.; DINARELLO, C.A.; MIER, J.W. IL-6 and APPs: anti-inflammatory and immunosuppressive mediators. Immunology, v. 18, p. 428-432, 1997. TODD, A.J. Anatomy of primary afferents and projection neurones inthe rat spinal dorsal horn with particular emphasis on substance Pand the neurokinin 1 receptor. Experimental Physiology, v. 87, p. 245-249, 2002. TRACEY, I.; MANTYH, P.W. The cerebral signature for pain perception and its modulation. Neuron, v. 55, p. 377–391, 2007. TRUNE, D.R.; LARRAIN, B.E.; HAUSMAN, F.A., KEMPTON, J.B., MACARTHUR, C.J. Simultaneous measurement of multiple ear proteins with multiplex ELISA assays. Hearing Research, v. 275, p. 1-7, 2011. TUNON DE LARA, J.M.; OKAYAMA, Y.; MCEUEN, A.R.; HEUSSER, C.H.; CHURCH, M.K.; WALLS, A.F. Release and inactivation of interleukin-4 by mast cells. Annals of the New York Academy of Sciences, v. 725, p.50-58, 2004. UCEYLER, N., SCHAFERS, M., SOMMER, C. Mode of action of cytokines on nociceptive neurons. Experimental Brain Research, v. 196, p. 67-78, 2009. UCEYLER, N.; TSCHARKE, A.; SOMMER, C. Early cytokine expression in mouse sciatic nerve after chronic constriction nerve injury depends on calpain. Brain Behavour, Immunity, v. 21, p. 553–560, 2007. VALE, M.L.; MARQUES, J.B.; MOREIRA, C.A.; ROCHA, F.A.; FERREIRA, S.H., POOLE, S., CUNHA, F.Q., RIBEIRO, R.A. Antinociceptive effects of interleukin-4, - 10, and -13 on the writhing response in mice and zymosan-induced knee joint incapacitation in rats. Journal of Pharmacological and Experimental Therapeutics, v. 304, p. 102-108, 2003. VAN DAMME, J.; CAYPHAS, S.; VAN SNICK, J.; CONINGS, R.; PUT, W.; LENAERTS, J. P.; SIMPSON, R. J.; BILLIAU, A. Purification and characterization of human fibroblast-derived hybridoma growth factor identical to T-cell-derived B-cell stimulatory factor-2 (interleukin-6). European Journal of Biochemistry, v. 168, p. 543-550, 1987. VANNIER, E.; MILLER, L.C.; DINARELLO, C.A. Coordinated antiinflammatory effects of interleukin 4: interleukin 4 suppresses interleukin 1 production but up-regulates gene expression and synthesis of interleukin 1 receptor antagonist. Proceedings of the 41 National Academy of Sciences of the United States of America USA, v. 89, p. 4076-4080, 1992. WAGNER, R.; JANJIGIAN, M.; MYERS, R.R. Anti-inflammatory interleukin-10 therapy in CCI neuropathy decreases thermal hyperalgesia, macrophage recruitment, and endoneurial TNF-alpha expression. Pain, v. 74, p. 35–42, 1998. WANG, Y.; FENG, C.; WU, Z.; WU, A.; YUE. Y. Activity of the descending noradrenergic pathway after surgery in rats. Acta Anaesthesiologica Scandinava, v. 52, p. 1336-1341, 2008. WEN Y.R.; SUTER, M.R.; JI, R.R., YEH, G.C.; WU, Y.S.; WANG, K.C.; KOHNO, T.; SUN, W.Z.; WANG, C.C. Activation of p38 mitogen-activated protein kinase in spinal microglia contributes to incision-induced mechanical allodynia. Anesthesiology, v. 110, p. 155-165, 2009. WHITESIDE, G. T.; HARRISON, J.; BOULET, J.; MARK, L.; PEARSON, M.; GOTTSHALL, S.; WALKER, K. Pharmacological characterisation of a rat model of incisional pain. British Journal of Pharmacology, v. 14, p. 85-91, 2004. WOLF, G.; LIVSHITS, D.; BEILIN, B.; YIRMIYA, R.; SHAVIT, Y. Interleukin- 1 signaling is required for induction and maintenance of postoperative incisional pain: genetic and pharmacological studies in mice. Brain, Behaviour, and Immunity, v. 22, p. 1072-1077, 2008. WOOLF, C.J. Recent advances in the pathophysiology of acute pain. British Journal of Anaesthesia, v. 63, p. 139-146, 1989. WOOLF, C.J.; CHONG, M.S. Preemptive analgesia – treating postoperative pain by prevention the establishment of central sensitization. Anesthesia & Analgalgesia, v. 177, p. 362-379, 1993. WOOLF, C.J.; SHORTLAND, P.; COGGESHALL, R.E. Peripheral-nerve injury triggers central sprouting of myelinated afferents. Nature, v. 355, p. 75-78, 1992. YAMAMOTO, N.; SAKAI, F.; YAMAZAKI, H.; NAKAHARA, K.; OKUHARA, M. Effect of FR167653, a cytokine suppressive agent, on endotoxin-induced disseminated intravascular coagulation. European Journal of Pharmacology, v. 314, p. 137-142, 1996. YAMAMOTO, N.; SAKAI, F.; YAMAZAKI, H.; SATO, N.; NAKAHARA, K.; OKUHARA, M. FR167653, a dual inhibitor of interleukin-1 and tumor necrosis factoralpha, ameliorates endotoxin-induced shock. European Journal of Pharmacology, v. 327, p. 169-174, 1997. ZAHN, P.K.; POGATZKI, E.M.; BRENNAN, T.J. Mechanisms for pain caused by incisions. Regional Anesthesia and Pain Medicine, v. 27, p. 514-516, 2002. ZHANG, J.; CHEN, L.; SU, T.; CAO, F.; MENG, X.; PEI, L.; SHI, J.; PAN, H. L.; LI, M. Electroacupuncture increases CB2 receptor expression on keratinocytes and infiltrating inflammatory cells in inflamed skin tissues of rats. Journal of Pain, v. 11, p. 1250-1258, 2010. 42 ZHU, X.; VINCLER, M.A.; PARKER, R.; EISENACH, J.C. Spinal cord dynorphin expression increases, but does not drive microglial prostaglandin production or mechanical hypersensitivity after incisional surgery in rats. Pain, v. 125, 43-52, 2006. ZIMMERMANN, M. Ethical guidelines for investigations of experimental pain in conscious animals Pain, v. 16, p. 109-110, 1983.https://tede.ufrrj.br/retrieve/60149/2012%20-%20Ligia%20Lins%20de%20Castro.pdf.jpghttps://tede.ufrrj.br/jspui/handle/jspui/3592Submitted by Sandra Pereira (srpereira@ufrrj.br) on 2020-06-01T20:49:58Z No. of bitstreams: 1 2012 - Ligia Lins de Castro.pdf: 1430306 bytes, checksum: 8fd4576cb38ca178198022a8d5deeeb1 (MD5)Made available in DSpace on 2020-06-01T20:49:58Z (GMT). No. of bitstreams: 1 2012 - Ligia Lins de Castro.pdf: 1430306 bytes, checksum: 8fd4576cb38ca178198022a8d5deeeb1 (MD5) Previous issue date: 2012-07-05info:eu-repo/semantics/openAccessreponame:Biblioteca Digital de Teses e Dissertações da UFRRJinstname:Universidade Federal Rural do Rio de Janeiro (UFRRJ)instacron:UFRRJTHUMBNAIL2012 - Ligia Lins de Castro.pdf.jpgGenerated Thumbnailimage/jpeg2104https://rima.ufrrj.br/jspui/bitstream/20.500.14407/14929/1/2012%20-%20Ligia%20Lins%20de%20Castro.pdf.jpgc4715912a635b5fbde63d2a9b070733fMD51TEXT2012 - Ligia Lins de Castro.pdf.txtExtracted Texttext/plain111279https://rima.ufrrj.br/jspui/bitstream/20.500.14407/14929/2/2012%20-%20Ligia%20Lins%20de%20Castro.pdf.txt0fe1f6a0ef485126952593d2e6033dc8MD52ORIGINAL2012 - Ligia Lins de Castro.pdf2012 - Ligia Lins de Castroapplication/pdf1430306https://rima.ufrrj.br/jspui/bitstream/20.500.14407/14929/3/2012%20-%20Ligia%20Lins%20de%20Castro.pdf8fd4576cb38ca178198022a8d5deeeb1MD53LICENSElicense.txttext/plain2089https://rima.ufrrj.br/jspui/bitstream/20.500.14407/14929/4/license.txt7b5ba3d2445355f386edab96125d42b7MD5420.500.14407/149292023-12-22 00:08:29.601oai:rima.ufrrj.br:20.500.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Biblioteca Digital de Teses e Dissertaçõeshttps://tede.ufrrj.br/PUBhttps://tede.ufrrj.br/oai/requestbibliot@ufrrj.br||bibliot@ufrrj.bropendoar:2023-12-22T03:08:29Biblioteca Digital de Teses e Dissertações da UFRRJ - Universidade Federal Rural do Rio de Janeiro (UFRRJ)false |
dc.title.por.fl_str_mv |
Investigação da participação de citocinas inflamatórias na medula espinhal de ratos na dor pós-incisional |
dc.title.alternative.eng.fl_str_mv |
Investigation of the involvement of inflammatory cytokines in rat spinal cord in incisional pain |
title |
Investigação da participação de citocinas inflamatórias na medula espinhal de ratos na dor pós-incisional |
spellingShingle |
Investigação da participação de citocinas inflamatórias na medula espinhal de ratos na dor pós-incisional Castro, Ligia Lins de dor pós-operatória nocicepção citocinas postoperative pain nociception cytokines Fisiologia |
title_short |
Investigação da participação de citocinas inflamatórias na medula espinhal de ratos na dor pós-incisional |
title_full |
Investigação da participação de citocinas inflamatórias na medula espinhal de ratos na dor pós-incisional |
title_fullStr |
Investigação da participação de citocinas inflamatórias na medula espinhal de ratos na dor pós-incisional |
title_full_unstemmed |
Investigação da participação de citocinas inflamatórias na medula espinhal de ratos na dor pós-incisional |
title_sort |
Investigação da participação de citocinas inflamatórias na medula espinhal de ratos na dor pós-incisional |
author |
Castro, Ligia Lins de |
author_facet |
Castro, Ligia Lins de |
author_role |
author |
dc.contributor.author.fl_str_mv |
Castro, Ligia Lins de |
dc.contributor.advisor1.fl_str_mv |
Medeiros, Magda Alves de |
dc.contributor.advisor1ID.fl_str_mv |
036592487-38 |
dc.contributor.advisor1Lattes.fl_str_mv |
http://lattes.cnpq.br/6392136073564306 |
dc.contributor.referee1.fl_str_mv |
Otero, Rosalia Mendez |
dc.contributor.referee2.fl_str_mv |
Vanderlinde, Frederico Argolo |
dc.contributor.authorID.fl_str_mv |
116286767-10 |
dc.contributor.authorLattes.fl_str_mv |
http://lattes.cnpq.br/6814868899883558 |
contributor_str_mv |
Medeiros, Magda Alves de Otero, Rosalia Mendez Vanderlinde, Frederico Argolo |
dc.subject.por.fl_str_mv |
dor pós-operatória nocicepção citocinas |
topic |
dor pós-operatória nocicepção citocinas postoperative pain nociception cytokines Fisiologia |
dc.subject.eng.fl_str_mv |
postoperative pain nociception cytokines |
dc.subject.cnpq.fl_str_mv |
Fisiologia |
description |
As diversas modalidades de dor são geradas e mantidas por diferentes mecanismos fisiopatológicos, devendo ser estudadas independentemente. A dor pós-operatória é uma forma comum e única de dor aguda e apesar dos avanços em seu estudo, permanece subtratada. Por causa da persistência da dor mesmo após o uso de medicamentos antiinflamatórios e opioides, postulamos que as citocinas possam desempenhar papel chave na dor pós-cirúrgica. Por meio de dados obtidos de testes nociceptivos, analisamos a concentração de citocinas inflamatórias liberadas pelo segmento lombar da medula espinhal de ratos submetidos ao modelo de dor pós-operatória. No teste de von Frey e no teste de Hargreaves, utilizados para avaliar a hiperalgesia mecânica e térmica, respectivamente, os animais tiveram redução dos limiares de retirada 1 hora após a incisão plantar que pode observada até as 72 horas após a cirurgia, quando comparados com animais sem incisão. Com base nesses resultados, foram feitas análises da liberação das citocinas pró-inflamatórias IL- 1β, IL-6 e TNF-α e das citocinas anti-inflamatórias IL-10 e IL-4 liberadas pela região lombar da medula espinhal pelo método de quimiluminescência às 2, 4, 6, 8, 12, 24, 48 e 72 horas após a incisão plantar. Através da técnica de qRT-PCR, as expressões gênicas de IL-1β, TNF- α e GFAP também foram avaliadas nos tempos de 2, 6, 48 e 72 horas após a incisão. Não houve alteração da liberação de IL-1β, IL-6, TNF-α e IL-4. Ocorreu diminuição significativa da liberação de IL-10 48 horas após a incisão quando comparado aos animais não incisados. Não houve alteração da expressão gênica de IL-1β, no entanto foi observado um aumento da expressão de TNF-α e GFAP 6 horas após a incisão quando comparados com animais não submetidos à incisão plantar. A incisão plantar não parece alterar a liberação das citocinas IL-1β, IL-6, TNF-α e IL-4. A manutenção da dor pós-operatória não está associada a uma queda sustentada dos níveis de IL-10. O aumento da expressão de RNAm de TNF-α condiz com o aumento da expressão de RNAm de GFAP e indica possível papel dos astrócitos na liberação da citocina. Porém, a manutenção da dor pós-operatória não está associada a um aumento constante da expressão gênica de TNF-α. O papel da liberação desta citocina na medula espinal no modelo de dor pós-operatória, assim como a confirmação da participação dos astrócitos necessitam ser investigados. |
publishDate |
2012 |
dc.date.issued.fl_str_mv |
2012-07-05 |
dc.date.accessioned.fl_str_mv |
2023-12-22T03:08:29Z |
dc.date.available.fl_str_mv |
2023-12-22T03:08:29Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/masterThesis |
format |
masterThesis |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
CASTRO, Ligia Lins de. Investigação da participação de citocinas inflamatórias na medula espinhal de ratos na dor pós-incisional. 2012. 42 f. Dissertação (Mestrado Multicêntrico em Ciências Fisiológicas) - Instituto de Ciências Biológicas e da Saúde, Universidade Federal Rural do Rio de Janeiro, Seropédica - RJ, 2012. |
dc.identifier.uri.fl_str_mv |
https://rima.ufrrj.br/jspui/handle/20.500.14407/14929 |
identifier_str_mv |
CASTRO, Ligia Lins de. Investigação da participação de citocinas inflamatórias na medula espinhal de ratos na dor pós-incisional. 2012. 42 f. Dissertação (Mestrado Multicêntrico em Ciências Fisiológicas) - Instituto de Ciências Biológicas e da Saúde, Universidade Federal Rural do Rio de Janeiro, Seropédica - RJ, 2012. |
url |
https://rima.ufrrj.br/jspui/handle/20.500.14407/14929 |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.relation.references.por.fl_str_mv |
ALKAITIS, M.S.; SOLORZANO, C.; LANDRY, R. P.; PIOMELLI, D.; DELEO, J. A.; ROMERO-SANDOVAL, E.A. Evidence for a role of endocannabinoids, astrocytes and p38 phosphorylation in the resolution of postoperative pain. PLoS One, v. 5, p. 10891, 2010. AWATSUJI, H.; FURUKAWA, Y.; HIROTA, M.; MURAKAMI, Y.; NII, S. M.; FURUKAWA, S.; HAYASHI, K. Interleukin-4 and -5 as modulators of nerve growth factor synthesis/secretion in astrocytes. Journal of Neuroscience Research, v. 34, p. 539- 545, 1993. BEDBROOK, G.M. Injuries of the Thoracolumbar Spine with Neurological Symptoms, em: Vinken, P. J.; Bruyn, G. W. Handbook of Clinical Neurology, Amsterdam: North-Holland, 1976. p. 437 a 466. BISHOP, G.H.; LANDAU, W.M.; JONES, M.H. Evidence for a double peripheral pathway for pain. Science, v. 128, p. 712-714, 1958. BRENNAN, T.J.; VANDERMEULEN, E.P.; GEBHART, G.F. Characterization of a rat model of incisional pain. Pain, v. 64, p. 493-501, 1996. BRENNAN, T.J.; ZAHN, P.K.; POGATZKI, E.M. Mechanisms of incisional pain. Anesthesiology Clinics of North America, v. 23, p. 1-20, 2005. BRENNER, G. J.; JI, R.R.; SHAFFER, S.; WOOLF, C.J. Peripheral noxious stimulation induces phosphorylation of the NMDA receptor NR1 subunit at the PKCdependent site, serine-896, in spinal cord dorsal horn neurons. European Journal of Neuroscience, v. 20, p. 375-384, 2004. CAMPBELL, J.N.; RAJA, S.N.; COHEN, R.H. Peripheral Neural Mechanisms of Nociception, em: Wall, P.D.; Melzack, R. Textbook of Pain, Edimburgo: Churchill Livingstone, 1989. p. 22 a 45. CARSWELL, E.A.; OLD, L.J.; KASSEL, R.L. An endotoxin-induced serum factor that causes necrosis of tumors. Procedings of the National Academy of Sciences of the United States of America, v. 72, p. 3666-3670, 1975. CHAO, C.C.; MOLITOR, T.W.; HU, S. Neuroprotective role of IL-4 against activated microglia. Journal of Immunology, v. 151, p. 1473-1481, 1993. CHAORAN, W.; BOUSTANY, L.; LIANG, H.; BRENNAN, T.J. Nerve Growth Factor Expression after Plantar Incision in the Rat. Anesthesiology, v. 107, p. 128–135, 2007. CHEN, L.; ZHANG, J.; LI, F.; QIU, Y.; WANG, L.; LI, Y. H.; SHI, J.; PAN, H. L.; LI, M. Endogenous anandamide and cannabinoid receptor-2 contribute to electroacupuncture analgesia in rats. Journal of Pain, v. 10, p. 732-739, 2009. CSÓKA, B.; NÉMETH, Z.H.; VIRÁG, L.; GERGELY, P.; LEIBOVICH, S.J.; PACHER, P.; SUN, C.X.; BLACKBURN, M.R.; VIZI, E.S.; DEITCH, E.A.; HASKÓ, G. A2A adenosine receptors and C/EBPbeta are crucially required for IL-10 production by macrophages exposed to Escherichia coli. Blood, v. 110, p. 2685-2695, 2007. 35 CUNHA, F.Q.; POOLE, S.; LORENZETTI, B.B.; FERREIRA, S.H. The pivotal role of tumour necrosis factor alpha in the development of inflammatory hyperalgesia. British Journal of Pharmacology, v. 107, p. 660–664, 1992. CUNHA, F.Q.; POOLE, S.; LORENZETTI, B.B.; VEIGA, F.H.; FERREIRA, S.H. Cytokine- mediated inflammatory hyperalgesia limited by interleukin-4. British Journal of Pharmacology, v. 126, p. 45–50, 1999. CUNHA, J.M; CUNHA, F.Q; POOLE, S.; FERREIRA, S.H. Cytokinemediated inflammatory hyperalgesia limited by interleukin-1 receptor antagonist. British Journal of Pharmacology, v. 130, p. 1418-1824, 2000. CUNHA, T.M.; VERRI WA, J.R.; SILVA, J.S.; POOLE, S.; CUNHA, F. Q.; FERREIRA, S.H. A cascade of cytokines mediates mechanical inflammatory hypernociception in mice. Procedings of the National Academy of Sciences of the United States of America. v.102, p. 1755-1760, 2005. DA FONSECA PACHECO, D.; KLEIN, A.; DE CASTRO PEREZ, A.; DA FONSECA PACHECO, C.M.; DE FRANCISCHI, J.N., DUARTE, I.D. The mu-opioid receptor agonist morphine, but not agonists at delta- or kappa-opioid receptors, induces peripheral antinociception mediated by cannabinoid receptors. British Journal of Pharmacology, v. 154, p. 1143-1149, 2008. DINARELLO, C. A. Interleukin-1, interleukin-1 receptors and interleukin-1 receptor antagonist. International Rewiew Immunology, v. 16, p. 457-499, 1998. DINARELLO, C.A. Proinflammatory and anti-inflammatory cytokines as mediators in the pathogenesis of septic shock. Chest, v. 112, p. 321S-329S, 1997. D'MELLO, R.; DICKENSON, A.H. Spinal cord mechanisms of pain. British Journal of Anaesthesia, v. 101. p. 8-16, 2008. FENTON, M.J.; BURAS, J.A.; DONNELLY, R.P. IL-4 reciprocally regulates IL-1 and IL-1 receptor antagonist expression in human monocytes. Journal of Immunology, v. 149, p. 1283-1288, 1992. FERREIRA, S.H. Hiperalgesia inflamatórial, óxido nítrico y control periférico del dolor. RevLatino Americana de Dolor, v. 12, p. 6-17, 1995. FERREIRA, S.H.; LORENZETTI, B.B.; BRISTOW, A.F.; POOLE, S. Interleukin-1 beta as a potent hyperalgesic agent antagonized by a tripeptide analogue. Nature, v. 6184, p. 698-700, 1988. FU, D.; GUO, Q.; AI, Y.; CAI, H.; YAN, J.; DAÍ, R. Glial activation and segmental upregulation of interleukin-1beta (IL-1beta) in the rat spinal cord after surgical incision. Neurochemical Research, v. 31, p. 333-340, 2006. GAGLIESE, L.; MELZACK, R. Age differences in nociception and pain behaviours in the rat. Neuroscience and Biobehavioral Reviews, v. 24, p. 843-854, 2000. GUO, W.; ZOU, S.; GUAN, Y; IKEDA, T.; TAL, M.; DUBNER, R.; REN, K.; Tyrosine phosphorylation of the NR2B subunit of the NMDA receptor in the spinal cord during the development and maintenance of inflammatory hyperalgesia. Journal of Neuroscience, v. 22, p. 6208-6217, 2002. 36 HARGREAVES, K.; DUBNER, R.; BROWN, F., FLORES, C., JORIS, J. A new and sensitive method for measuring thermal nociception in cutaneous hyperalgesia. Pain, v. 32, p. 77-88, 1988. HASKO, G.; SZABO, C.; NEMETH, Z.H.; KVETAN, V.; PASTORES, S.M.; VIZI, E.S. Adenosine receptor agonists differentially regulate IL-10, TNF-alpha, and nitric oxide production in RAW 264.7 macrophages and in endotoxemic mice. Journal of Immunology, v. 157, p. 4634-4640. 1996. HUITINGA, I.; SCHMIDT, E.D.; VAN DER CAMMEN, M.J.; BINNEKADE, R.; TILDERS, F.J. Priming with inter- leukin-1beta suppresses experimental allergic encephalomyelitis in the Lewis rat. Journal of Neuroendocrinology, v. 12, p. 1186–1193, 2000. HUNT, S.P.; PINI, A.; EVAN, G. Induction of c-fos-like protein in spinal cord neurons following sensory stimulation. Nature, v. 328, p. 632-634, 1987. IBRAHIM, M.; PORRECA, F.; LAI, J.; ALBRECHT, P.J.; RICE, F.L.; KHODOROVA, A.; DAVAR, G.; MAKRIYANNIS, A.; VANDERAH, T.W.; MATA, H.P.; MALAN JR, F. CB2 cannabinoid receptor activation produces antinociception by stimulating peripheral release of endogenous opioids. PNAS, v. 102, p. 3093-3098, 2005. ISAACS, A. & LINDENMANN, J. Virus interference. I. The interferon. Journal of Interferon Research, v. 5, p. 429-438, 1957. ITO, N.; OBATA, H., SAITO, S. Spinal microglial expression and mechanical hypersensitivity in a postoperative pain model: comparison with a neuropathic pain model. Anesthesiology, v. 111, p. 640-648, 2009. JI, R.R.; SAMAD, T.A.; JIN, S.X. p38 MAPK activation by NGF in primary sensory neurons after inflammation increases TRPV1 levels and maintains heat hyperalgesia. Neuron, v. 36, p. 57-68, 2002. JI, R.R.; KOHNO, T.; MOORE, K.A. Central sensitization and LTP: do pain and memory share similar mechanisms? Trends of Neuroscience, v. 26, p. 696-705, 2003. JORDAN, M.; OTTERNESS, I.G.; NG, R.; GESSNER, A.; ROLLINGHOFF, M.; BEUSCHER, H.U. Neutralization of endogenous IL-6 suppresses induction of IL-1 receptor antagonist. Journal of Immunology, v. 154, p. 4081-4090, 1995. KANAAN, S.A.; POOLE, S.; SAADE, N.E.; JABBUR, S.; SAFIEHGARABEDIAN, B. Interleukin-10 reduces the endotoxin-induced hyperalgesia in mice. Journal of Neuroimmunology, v. 86, p. 142-150, 1998. KAWAKAMI, M.; CERAMI, A. Studies of endotoxin-induced decrease in lipoprotein lipase activity. The Journal of Experimental Medicine, v. 154, p. 6319, 1981. KAWASAKI, Y.; ZHANG, L.; CHENG, J.K.; JI, R.R. Cytokine mechanisms of central sensitization: distinct and overlapping role of interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha in regulating synaptic and neuronal activity in the superficial spinal cord. Journal of Neuroscience, v. 28, p. 5189–5194, 2008. 37 KAPLAN, M.D.; OLSCHOWKA, J.A.; O'BANION, M.K. Cyclooxygenase- 1 behaves as a delayed response gene in PC12 cells differentiated by nerve growth factor. The Journal of Biological Chemistry, v. 272, p. 534-537, 1997. KISSELEVA, T.; BHATTACHARYA, S.; BRAUNSTEIN, J.; SCHINDLER, C. W. Signaling through the JAK/STAT pathway, recent advances and future challenges. Gene, v. 285, p. 1-24, 2002. LAVICH, T.R.; CORDEIRO, R.S.B.; SILVA, P.M.R.; MARTINS, M.A. A novel hot-plate test sensitive to hyperalgesic stimuli and non-opioid analgesics. Brazilian Journal of Medical and Biological Research, v. 38, p. 445-451, 2005. LEDEBOER, A.; JEKICH B.M.; SLOANE, E.M.; MAHONEY, J.H.; LANGER, S.J.; MILIGAN, E.D. MARTIN, D.; MAIER, S.F.; JOHNSON, K.W.; LESLIE, A.; CHAVEZ, R.A.; WATKINGS, L.R. Intrathecal Interleukin-10 Gene Therapy Attenuates Paclitaxel Induced Mechanical Allodynia and Proinflammatory Cytokine Expression in Dorsal Root Ganglia in Rats. Brain, Behaviour, Immunity, v. 21, p. 686-698, 2007. LEE S.R.; GUO, S.Z.; SCANNEVIN, R.H.; MAGLIARO, B.C.; RHODES, K.J., WANG, X.; LO, E.H. Induction of matrix metalloproteinase, cytokines and chemokines in rat cortical astrocytes exposed to plasminogen activators. Neuroscience Letters, v. 417, p. 1-5, 2007. LEEM, J.W.; WILLIS, W.D.; CHUNG, J.M. Cutaneous sensory receptors in the rat foot. Journal of Neurophysiology, v. 69, p. 1684-1699, 1993. LI, C.; XU, J.; LIU, D.; ZHANG, J.; DAI, R. Brain derived neurotrophic factor (BDNF) contributes to the pain hypersensitivity following surgical incision in the rats. Molecular Pain, v. 4, p. 27, 2008. LI, X.; ANGST, M.S.; CLARK, J.D. Opioid-induced hyperalgesia and incisional pain. Anesthesia & Analgesia, v. 93, p. 204-209, 2001. LIANG, D.Y; SHI, X.; QIAO, X; ANGST, M.S.; YEOMANS C.D.; CLARK, J.D. Chronic morphine administration enhances nociceptive sensitivity and local cytokine production after incision. Molecular Pain, v. 4, p. 7, 2008. LOEWENSTEIN, W.R. Mechano-Electric Transduction in the Pacinian Corpuscle: Initiation of Sensory Impulses in Mechanoreceptors. Handbook of Sensory Physiology, Berlim: Springer-Verlag, 1971, p. 267 a 290. LORAM, L.C.; HARRISON, J.A.; SLOANE, E.M.; HUTCHINSON, M.R.; SHOLAR, P.; TAYLOR, F.R.; BERKELHAMMER, D.; COATS, B.D.; POOLE, S.; MILLIGAN, E.D.; MAIER, S.F.; RIEGER, J.; WATKINS, L.R. Enduring reversal of neuropathic pain by a single intrathecal injection of adenosine 2A receptor agonists: a novel therapy for neuropathic pain. Journal of Neuroscience, v. 29, p. 14015-14025, 2009. LORAM, L.C.; THEMISTOCLEOUS, A.C.; FICK, L.G.; KAMERMAN, P.R. The time course of inflammatory cytokine secretion in a rat model of postoperative pain does not coincide with the onset of mechanical hyperalgesia. Canadian Journal of Physiology and Pharmacology, v. 85, p. 613-620, 2007. LUCAS, S.M.; ROTHWELL, N.J.; GIBSON, R.M. The role of inflammation in CNS injury and disease. British Journal of Pharmacology, v. 147, p.S232-240, 2006. 38 MARCHAND, F.; PERRETI, M.; MC MAHON, S.B. Role of the immune system in chronic pain. Nature Reviews of Neuroscience, v. 6, p. 521-532, 2005. MILLER, A.J.; HOPKINS, S.J.; LUHESHI, G.N. Sites of action of IL-1 in the development of fever and cytokine responses to tissue inflammation in the rat. British Journal of Pharmacology, v. 120,p. 1274-1279, 1997. MÖLLER, K.A.; JOHANSSON, B.; BERGE, O.G. Assessing mechanical allodynia in the rat paw with a new electronic algometer. Journal of Neuroscience Methods, v. 84, p. 41-47, 1998. MOSSNER, R.; BECKMANN, I.; HALLERMANN, C.; NEUMANN, C.; REICH, K. Granulocyte colony-stimulating-factor-induced psoriasi form dermatitis resembles psoriasis with regard to abnormal cytokine expression and epidermal activation. Experimental Dermatology, v. 13, p. 340-346, 2004. NAKA, T.; NISHIMOTO, N.; KISHIMOTO, T. The paradigm of IL-6: from basic science to medicine. Arthritis Research, v. 4, p. S233-242, 2002. NICOLA, N. A.; NICHOLSON, S.E.; METCALF, D.; ZHANG, J.G.; BACA, M.; FARLEY, A.; WILLSON, T.A.; STARR, R.; ALEXANDER, W.; HILTON, D.J. Negative regulation of cytokine signaling by the SOCS proteins. Cold Spring Harbor Symposia Quantitative Biology, v. 64,p. 397-404, 1999. NODA, M.; NAKANISHI, H.; NABEKURA, J.; AKAIKE, N. AMPAkainate subtypes of glutamate receptor in rat cerebral microglia. Journal of Neuroscience, v. 20,p. 251-258, 2000. O’BANION, M.K. Cyclooxygenase-2: molecular biology, pharmacology, and neurobiology. Critical Reviews in Neurobiology, v. 13, p. 45-82, 1999. OBATA, H.; EISENACH, J.C.; HUSSAIN, H.; BYNUM, T.; VINCLER, M. Spinal Glial Activation Contributes to Postoperative Mechanical Hypersensitivity in the Rat. Journal of Pain, v. 7, p. 816-822, 2006. ONOE, Y.; MIYAURA, C.; KAMINAKAYASHIKI, T.; NAGAI, Y.; NOGUCHI, K.; CHEN, Q. R.; SEO, H.; OHTA, H. NOZAWA, S. KUDO, I.; SUDA, T. IL-13 and IL- 4 inhibit bone resorption by suppressing cyclooxygenase-2-dependent prostaglandin synthesis in osteoblasts. Journal of Immunology, v. 156, p. 758-764, 1996. PERKINS, M.N.; KELLY, D. Interleukin-1 beta induced-desArg9bradykininmediated thermal hyperalgesia in the rat. Neuropharmacology, vol. 5: p. 657-660, 1994. PIOTROWSKI, W.; FOREMAN, J.C. Some effects of calcitonin generelated peptide in human skin and on histamine release. British Journal of Dermatology, v. 114, p.37-46, 1986. POGATZKI, E.M.; GEBHART, G.F.; BRENNAN, T.J. Characterization of A- and C-fibers innervating the plantar rathindpaw one day after an incision. Journal of Neurophisiology, v. 87, p. 721-731, 2001. POGATZKI, E.M.; ZAHN, P.K.; BRENNAN, T.J. Postoperative pain-clinical implications of basic research. Best Practice & Research: Clinical Anaesthesiology, v. 21, p. 3-13, 2007. 39 POOLE, S.; CUNHA, F.Q.; SELKIRK, S.; LORENZETTI, B.B.; FERREIRA, S.H. Cytokine-mediated inflammatory hyperalgesia limited by interleukin-10. British Journal of Pharmacology, v. 115, p. 684-688, 1995. POOLE, S.; LORENZETTI, B.B.; CUNHA, J.M.; CUNHA, F.Q.; FERREIRA, S.H. Bradykinin B1 and B2 receptors, tumour necrosis factor alpha and inflammatory hyperalgesia. British Journal of Pharmacology, v. 126, p. 649-56, 1999. RANDIC, M. JIANG, M.C.; CERNE, R. Long-term potentiation and long term depression of primary afferent neurotransmission in the rat spinal cord. Journal of Neuroscience, v. 13, p. 5228-5241, 1993. REICHL, S.; AUGUSTIN, M.; ZAHN, P.K.; POGATZKI-ZAHN, E.M. Peripheral and spinal GABAergic regulation of incisional pain in rats. Pain, v. 153, p. 129-141, 2012. ROCHA, A.P.C.; KRAYCHETE, D.C.; LEMONICA, L.; CARVALHO, L.R.; BARROS, G.A.M.; GARCIA, J.B.S.; SAKATA, R.K. Dor: Aspectos Atuais da Sensibilização Periférica e Central. Revista Brasileira de Anestesiologia, v. 57, p. 94-105, 2007. ROMERO-SANDOVAL, A.; CHAI, N.; NUTILE-MCMENEMY, N.; DELEO, J.A. A comparison of spinal Iba1 and GFAP expression in rodent models of acute and chronic pain. Brain Research, v. 1219, p. 116-26, 2008. ROMERO-SANDOVAL, A.;EISENACH, J.C. Spinal cannabinoid receptor type 2 activation reduces hypersensitivity and spinal cord glial activation after paw incision. Anesthesiology, v. 106, p. 787-794, 2007. SANDKUHLER, J. Learning and memory in pain pathways. Pain, v. 88, p. 113-118, 2000. SCHAFERS, M.; SOMMER, C.; GEIS, C.; HAGENACKER, T.; VANDENABEELE, P.; SORKIN, L.S. Selective stimulation of either tumor necrosis factor receptor differentially induces pain behavior in vivo and ectopic activity in sensory neurons in vitro. Neuroscience, v. 157, p. 414-423, 2008. SCHAFERS, M.; SORKIN, L.S.; GEIS, C. SHUBAYEV. V.I. Spinal nerve ligation induces transient upregulation of tumor necrosis factor receptors 1 and 2 in injured and adjacent uninjured dorsal root ganglia in the rat. Neuroscience Letters, v. 347, p. 179-182, 2003. SHUAI, K. & LIU, B. Regulation of JAK–STAT signalling in the immune system. Nature Reviews Immunology, v. 3, p. 900-911, 2003. SPRANGER, M.; LINDHOLM, D.; BANDTLOW, C.; HEUMANN, R.; GNAHN, H. NTIER- NOE, M.; THOENEN, H. Regulation o f nerve growth factor (NGF) synthesis in the rat central nervous system: comparison between the effects o f interleukin- 1 and various growth factors in astrocyte cultures and in vivo. European Journal of Neuroscience, v. 2, p. 69-76, 1990. STARR, R. & HILTON, D.J. Negative regulation of the JAK/STAT pathway. Bioessays, v. 1, p. 47-52, 1999. 40 STELLWAGEN, D.; BEATTIE, E.C.; SEO, J.Y.; MALENKA, R.C. Differential regulation of AMPA receptor and GABA receptor trafficking by tumor necrosis factoralpha. Journal of Neuroscience, v. 25, p. 3219–3228, 2005. STRLE, K.; ZHOU, J.H.; SHEN, W.H.; BROUSSARD, S.R.; JOHNSON, R.W.; FREUND, G.G.; DANTZER, R.; KELLEY, K.W. Interleukin-10 in the brain. Critical Revewies in Immunology, v. 21, p. 427–449, 2001. SU, T.F.; ZHAO, Y.Q.; ZHANG, L.H.; PENG, M.; WU, C. H.; PEI, L.; TIAN, B., ZHANG, J.; SHI, J.; PAN, H.L.; LI, M. Electroacupuncture reduces the expression of proinflammatory cytokines in inflamed skin tissues through activation of cannabinoid CB2 receptors. European Journal of Pain, v. 16, p. 624-35, 2012. TILG, H.; DINARELLO, C.A.; MIER, J.W. IL-6 and APPs: anti-inflammatory and immunosuppressive mediators. Immunology, v. 18, p. 428-432, 1997. TODD, A.J. Anatomy of primary afferents and projection neurones inthe rat spinal dorsal horn with particular emphasis on substance Pand the neurokinin 1 receptor. Experimental Physiology, v. 87, p. 245-249, 2002. TRACEY, I.; MANTYH, P.W. The cerebral signature for pain perception and its modulation. Neuron, v. 55, p. 377–391, 2007. TRUNE, D.R.; LARRAIN, B.E.; HAUSMAN, F.A., KEMPTON, J.B., MACARTHUR, C.J. Simultaneous measurement of multiple ear proteins with multiplex ELISA assays. Hearing Research, v. 275, p. 1-7, 2011. TUNON DE LARA, J.M.; OKAYAMA, Y.; MCEUEN, A.R.; HEUSSER, C.H.; CHURCH, M.K.; WALLS, A.F. Release and inactivation of interleukin-4 by mast cells. Annals of the New York Academy of Sciences, v. 725, p.50-58, 2004. UCEYLER, N., SCHAFERS, M., SOMMER, C. Mode of action of cytokines on nociceptive neurons. Experimental Brain Research, v. 196, p. 67-78, 2009. UCEYLER, N.; TSCHARKE, A.; SOMMER, C. Early cytokine expression in mouse sciatic nerve after chronic constriction nerve injury depends on calpain. Brain Behavour, Immunity, v. 21, p. 553–560, 2007. VALE, M.L.; MARQUES, J.B.; MOREIRA, C.A.; ROCHA, F.A.; FERREIRA, S.H., POOLE, S., CUNHA, F.Q., RIBEIRO, R.A. Antinociceptive effects of interleukin-4, - 10, and -13 on the writhing response in mice and zymosan-induced knee joint incapacitation in rats. Journal of Pharmacological and Experimental Therapeutics, v. 304, p. 102-108, 2003. VAN DAMME, J.; CAYPHAS, S.; VAN SNICK, J.; CONINGS, R.; PUT, W.; LENAERTS, J. P.; SIMPSON, R. J.; BILLIAU, A. Purification and characterization of human fibroblast-derived hybridoma growth factor identical to T-cell-derived B-cell stimulatory factor-2 (interleukin-6). European Journal of Biochemistry, v. 168, p. 543-550, 1987. VANNIER, E.; MILLER, L.C.; DINARELLO, C.A. Coordinated antiinflammatory effects of interleukin 4: interleukin 4 suppresses interleukin 1 production but up-regulates gene expression and synthesis of interleukin 1 receptor antagonist. Proceedings of the 41 National Academy of Sciences of the United States of America USA, v. 89, p. 4076-4080, 1992. WAGNER, R.; JANJIGIAN, M.; MYERS, R.R. Anti-inflammatory interleukin-10 therapy in CCI neuropathy decreases thermal hyperalgesia, macrophage recruitment, and endoneurial TNF-alpha expression. Pain, v. 74, p. 35–42, 1998. WANG, Y.; FENG, C.; WU, Z.; WU, A.; YUE. Y. Activity of the descending noradrenergic pathway after surgery in rats. Acta Anaesthesiologica Scandinava, v. 52, p. 1336-1341, 2008. WEN Y.R.; SUTER, M.R.; JI, R.R., YEH, G.C.; WU, Y.S.; WANG, K.C.; KOHNO, T.; SUN, W.Z.; WANG, C.C. Activation of p38 mitogen-activated protein kinase in spinal microglia contributes to incision-induced mechanical allodynia. Anesthesiology, v. 110, p. 155-165, 2009. WHITESIDE, G. T.; HARRISON, J.; BOULET, J.; MARK, L.; PEARSON, M.; GOTTSHALL, S.; WALKER, K. Pharmacological characterisation of a rat model of incisional pain. British Journal of Pharmacology, v. 14, p. 85-91, 2004. WOLF, G.; LIVSHITS, D.; BEILIN, B.; YIRMIYA, R.; SHAVIT, Y. Interleukin- 1 signaling is required for induction and maintenance of postoperative incisional pain: genetic and pharmacological studies in mice. Brain, Behaviour, and Immunity, v. 22, p. 1072-1077, 2008. WOOLF, C.J. Recent advances in the pathophysiology of acute pain. British Journal of Anaesthesia, v. 63, p. 139-146, 1989. WOOLF, C.J.; CHONG, M.S. Preemptive analgesia – treating postoperative pain by prevention the establishment of central sensitization. Anesthesia & Analgalgesia, v. 177, p. 362-379, 1993. WOOLF, C.J.; SHORTLAND, P.; COGGESHALL, R.E. Peripheral-nerve injury triggers central sprouting of myelinated afferents. Nature, v. 355, p. 75-78, 1992. YAMAMOTO, N.; SAKAI, F.; YAMAZAKI, H.; NAKAHARA, K.; OKUHARA, M. Effect of FR167653, a cytokine suppressive agent, on endotoxin-induced disseminated intravascular coagulation. European Journal of Pharmacology, v. 314, p. 137-142, 1996. YAMAMOTO, N.; SAKAI, F.; YAMAZAKI, H.; SATO, N.; NAKAHARA, K.; OKUHARA, M. FR167653, a dual inhibitor of interleukin-1 and tumor necrosis factoralpha, ameliorates endotoxin-induced shock. European Journal of Pharmacology, v. 327, p. 169-174, 1997. ZAHN, P.K.; POGATZKI, E.M.; BRENNAN, T.J. Mechanisms for pain caused by incisions. Regional Anesthesia and Pain Medicine, v. 27, p. 514-516, 2002. ZHANG, J.; CHEN, L.; SU, T.; CAO, F.; MENG, X.; PEI, L.; SHI, J.; PAN, H. L.; LI, M. Electroacupuncture increases CB2 receptor expression on keratinocytes and infiltrating inflammatory cells in inflamed skin tissues of rats. Journal of Pain, v. 11, p. 1250-1258, 2010. 42 ZHU, X.; VINCLER, M.A.; PARKER, R.; EISENACH, J.C. Spinal cord dynorphin expression increases, but does not drive microglial prostaglandin production or mechanical hypersensitivity after incisional surgery in rats. Pain, v. 125, 43-52, 2006. ZIMMERMANN, M. Ethical guidelines for investigations of experimental pain in conscious animals Pain, v. 16, p. 109-110, 1983. |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Universidade Federal Rural do Rio de Janeiro |
dc.publisher.program.fl_str_mv |
Programa Multicêntrico de Pós-Graduação em Ciências Fisiológicas |
dc.publisher.initials.fl_str_mv |
UFRRJ |
dc.publisher.country.fl_str_mv |
Brasil |
dc.publisher.department.fl_str_mv |
Instituto de Ciências Biológicas e da Saúde |
publisher.none.fl_str_mv |
Universidade Federal Rural do Rio de Janeiro |
dc.source.none.fl_str_mv |
reponame:Biblioteca Digital de Teses e Dissertações da UFRRJ instname:Universidade Federal Rural do Rio de Janeiro (UFRRJ) instacron:UFRRJ |
instname_str |
Universidade Federal Rural do Rio de Janeiro (UFRRJ) |
instacron_str |
UFRRJ |
institution |
UFRRJ |
reponame_str |
Biblioteca Digital de Teses e Dissertações da UFRRJ |
collection |
Biblioteca Digital de Teses e Dissertações da UFRRJ |
bitstream.url.fl_str_mv |
https://rima.ufrrj.br/jspui/bitstream/20.500.14407/14929/1/2012%20-%20Ligia%20Lins%20de%20Castro.pdf.jpg https://rima.ufrrj.br/jspui/bitstream/20.500.14407/14929/2/2012%20-%20Ligia%20Lins%20de%20Castro.pdf.txt https://rima.ufrrj.br/jspui/bitstream/20.500.14407/14929/3/2012%20-%20Ligia%20Lins%20de%20Castro.pdf https://rima.ufrrj.br/jspui/bitstream/20.500.14407/14929/4/license.txt |
bitstream.checksum.fl_str_mv |
c4715912a635b5fbde63d2a9b070733f 0fe1f6a0ef485126952593d2e6033dc8 8fd4576cb38ca178198022a8d5deeeb1 7b5ba3d2445355f386edab96125d42b7 |
bitstream.checksumAlgorithm.fl_str_mv |
MD5 MD5 MD5 MD5 |
repository.name.fl_str_mv |
Biblioteca Digital de Teses e Dissertações da UFRRJ - Universidade Federal Rural do Rio de Janeiro (UFRRJ) |
repository.mail.fl_str_mv |
bibliot@ufrrj.br||bibliot@ufrrj.br |
_version_ |
1810108176224223232 |