Cardioprotective Effect of Cilostazol on Ischemia-Reperfusion Injury Model

Detalhes bibliográficos
Autor(a) principal: Sahin,Mazlum
Data de Publicação: 2022
Outros Autores: Baytaroglu,Corc, Sevgili,Emrah
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Brazilian Journal of Cardiovascular Surgery (Online)
Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-76382022000600843
Resumo: Abstract Introduction: To clarify the potential protective role of cilostazol on rat myocardial cells with ischemia-reperfusion injury (IRI) models. Methods: The study was conducted with three groups of 10 Wistar rats (control group, rats without any coronary ischemia; sham group, rats with coronary ischemia but without cilostazol administration; and cilostazol group, rats with coronary ischemia and cilostazol administration). The level of myocardial injuries was measured by analyzing cardiac troponin T and creatine kinase MB levels in blood samples. In tissue samples, adenosine triphosphate (ATP), nitric oxide, superoxide dismutase (SOD), and malondialdehyde were used to determine the amount of tissue damage. Tissues were stained with hematoxylin-eosin method, and samples were examined under light microscope. Results: The mean level of ATP was 104.4 in the cilostazol group and 149.1 in the sham group (P=0.044). SOD level was significantly higher in the cilostazol group than in the sham group (2075.3 vs. 1783.7, P=0.043). According to histopathological examination, all samples were classified as G0 in the control group. In the sham group, one sample was categorized as G1, six samples as G2, and three samples as G3. In the cilostazol group, nine samples and one sample were categorized as G1 and G2, respectively (P=0.011). Conclusion: Cilostazol has beneficial effects on Wistar rats’ myocardial cells in regard to decreasing inflammatory process, necrosis, and fibrosis. Our findings revealed that the use of cilostazol significantly decreased ATP and increased SOD levels in Wistar rats’ myocardial cells after IRI.
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spelling Cardioprotective Effect of Cilostazol on Ischemia-Reperfusion Injury ModelAdenosine TriphosphateCilostazolInflammationMyocardial IschemiaSuperoxide DismutaseAbstract Introduction: To clarify the potential protective role of cilostazol on rat myocardial cells with ischemia-reperfusion injury (IRI) models. Methods: The study was conducted with three groups of 10 Wistar rats (control group, rats without any coronary ischemia; sham group, rats with coronary ischemia but without cilostazol administration; and cilostazol group, rats with coronary ischemia and cilostazol administration). The level of myocardial injuries was measured by analyzing cardiac troponin T and creatine kinase MB levels in blood samples. In tissue samples, adenosine triphosphate (ATP), nitric oxide, superoxide dismutase (SOD), and malondialdehyde were used to determine the amount of tissue damage. Tissues were stained with hematoxylin-eosin method, and samples were examined under light microscope. Results: The mean level of ATP was 104.4 in the cilostazol group and 149.1 in the sham group (P=0.044). SOD level was significantly higher in the cilostazol group than in the sham group (2075.3 vs. 1783.7, P=0.043). According to histopathological examination, all samples were classified as G0 in the control group. In the sham group, one sample was categorized as G1, six samples as G2, and three samples as G3. In the cilostazol group, nine samples and one sample were categorized as G1 and G2, respectively (P=0.011). Conclusion: Cilostazol has beneficial effects on Wistar rats’ myocardial cells in regard to decreasing inflammatory process, necrosis, and fibrosis. Our findings revealed that the use of cilostazol significantly decreased ATP and increased SOD levels in Wistar rats’ myocardial cells after IRI.Sociedade Brasileira de Cirurgia Cardiovascular2022-12-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-76382022000600843Brazilian Journal of Cardiovascular Surgery v.37 n.6 2022reponame:Brazilian Journal of Cardiovascular Surgery (Online)instname:Sociedade Brasileira de Cirurgia Cardiovascular (SBCCV)instacron:SBCCV10.21470/1678-9741-2020-0651info:eu-repo/semantics/openAccessSahin,MazlumBaytaroglu,CorcSevgili,Emraheng2022-11-22T00:00:00Zoai:scielo:S0102-76382022000600843Revistahttp://www.rbccv.org.br/https://old.scielo.br/oai/scielo-oai.php||rosangela.monteiro@incor.usp.br|| domingo@braile.com.br|| brandau@braile.com.br1678-97410102-7638opendoar:2022-11-22T00:00Brazilian Journal of Cardiovascular Surgery (Online) - Sociedade Brasileira de Cirurgia Cardiovascular (SBCCV)false
dc.title.none.fl_str_mv Cardioprotective Effect of Cilostazol on Ischemia-Reperfusion Injury Model
title Cardioprotective Effect of Cilostazol on Ischemia-Reperfusion Injury Model
spellingShingle Cardioprotective Effect of Cilostazol on Ischemia-Reperfusion Injury Model
Sahin,Mazlum
Adenosine Triphosphate
Cilostazol
Inflammation
Myocardial Ischemia
Superoxide Dismutase
title_short Cardioprotective Effect of Cilostazol on Ischemia-Reperfusion Injury Model
title_full Cardioprotective Effect of Cilostazol on Ischemia-Reperfusion Injury Model
title_fullStr Cardioprotective Effect of Cilostazol on Ischemia-Reperfusion Injury Model
title_full_unstemmed Cardioprotective Effect of Cilostazol on Ischemia-Reperfusion Injury Model
title_sort Cardioprotective Effect of Cilostazol on Ischemia-Reperfusion Injury Model
author Sahin,Mazlum
author_facet Sahin,Mazlum
Baytaroglu,Corc
Sevgili,Emrah
author_role author
author2 Baytaroglu,Corc
Sevgili,Emrah
author2_role author
author
dc.contributor.author.fl_str_mv Sahin,Mazlum
Baytaroglu,Corc
Sevgili,Emrah
dc.subject.por.fl_str_mv Adenosine Triphosphate
Cilostazol
Inflammation
Myocardial Ischemia
Superoxide Dismutase
topic Adenosine Triphosphate
Cilostazol
Inflammation
Myocardial Ischemia
Superoxide Dismutase
description Abstract Introduction: To clarify the potential protective role of cilostazol on rat myocardial cells with ischemia-reperfusion injury (IRI) models. Methods: The study was conducted with three groups of 10 Wistar rats (control group, rats without any coronary ischemia; sham group, rats with coronary ischemia but without cilostazol administration; and cilostazol group, rats with coronary ischemia and cilostazol administration). The level of myocardial injuries was measured by analyzing cardiac troponin T and creatine kinase MB levels in blood samples. In tissue samples, adenosine triphosphate (ATP), nitric oxide, superoxide dismutase (SOD), and malondialdehyde were used to determine the amount of tissue damage. Tissues were stained with hematoxylin-eosin method, and samples were examined under light microscope. Results: The mean level of ATP was 104.4 in the cilostazol group and 149.1 in the sham group (P=0.044). SOD level was significantly higher in the cilostazol group than in the sham group (2075.3 vs. 1783.7, P=0.043). According to histopathological examination, all samples were classified as G0 in the control group. In the sham group, one sample was categorized as G1, six samples as G2, and three samples as G3. In the cilostazol group, nine samples and one sample were categorized as G1 and G2, respectively (P=0.011). Conclusion: Cilostazol has beneficial effects on Wistar rats’ myocardial cells in regard to decreasing inflammatory process, necrosis, and fibrosis. Our findings revealed that the use of cilostazol significantly decreased ATP and increased SOD levels in Wistar rats’ myocardial cells after IRI.
publishDate 2022
dc.date.none.fl_str_mv 2022-12-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-76382022000600843
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-76382022000600843
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.21470/1678-9741-2020-0651
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv text/html
dc.publisher.none.fl_str_mv Sociedade Brasileira de Cirurgia Cardiovascular
publisher.none.fl_str_mv Sociedade Brasileira de Cirurgia Cardiovascular
dc.source.none.fl_str_mv Brazilian Journal of Cardiovascular Surgery v.37 n.6 2022
reponame:Brazilian Journal of Cardiovascular Surgery (Online)
instname:Sociedade Brasileira de Cirurgia Cardiovascular (SBCCV)
instacron:SBCCV
instname_str Sociedade Brasileira de Cirurgia Cardiovascular (SBCCV)
instacron_str SBCCV
institution SBCCV
reponame_str Brazilian Journal of Cardiovascular Surgery (Online)
collection Brazilian Journal of Cardiovascular Surgery (Online)
repository.name.fl_str_mv Brazilian Journal of Cardiovascular Surgery (Online) - Sociedade Brasileira de Cirurgia Cardiovascular (SBCCV)
repository.mail.fl_str_mv ||rosangela.monteiro@incor.usp.br|| domingo@braile.com.br|| brandau@braile.com.br
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