The Neuroprotective Effects of Ginsenoside Rd Pretreatment in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , |
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=S0102-76382022005007206 |
Resumo: | ABSTRACT Introduction: Paraplegia may develop as a result of spinal cord ischemia-reperfusion injury in patients who underwent thoracoabdominal aortic surgery. The objective of this research is to determine the neuroprotective effects of ginsenoside Rd pretreatment in a rat model of spinal cord ischemia-reperfusion injury. Methods: Sprague-Dawley rats (n=36) were randomly assigned to three groups. The sham (n=12) and control (n=12) groups received normal saline orally. The Rd group (n=12) received ginsenoside Rd (100 mg/kg) orally 48 hours before the induction of spinal cord ischemia. Spinal cord ischemia was induced by aortic occlusion using a Fogarty balloon catheter in the Rd and control groups. A neurological assessment according to the motor deficit index and a histological evaluation of the spinal cord were performed. To evaluate the antioxidant activity of ginsenoside Rd, malondialdehyde levels and superoxide dismutase activity were determined. Further, the tissue levels of tumor necrosis factor-alpha and interleukin-1 beta were measured. Results: The Rd group showed significantly lower motor deficit index scores than did the control group throughout the entire experimental period (P<0.001). The Rd group demonstrated significantly greater numbers of normal motor neurons than did the control group (P=0.039). The Rd group exhibited decreased malondialdehyde levels (P<0.001) and increased superoxide dismutase activity (P=0.029) compared to the control group. Tumor necrosis factor-alpha and interleukin-1 beta tissue levels were significantly decreased in the Rd group (P<0.001). Conclusion: Ginsenoside Rd pretreatment may be a promising treatment to prevent ischemia-reperfusion injury in patients who undergo thoracoabdominal aortic surgery. |
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Brazilian Journal of Cardiovascular Surgery (Online) |
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The Neuroprotective Effects of Ginsenoside Rd Pretreatment in a Rat Model of Spinal Cord Ischemia-Reperfusion InjuryGinsenosidesSpinal CordParaplegiaNeuroprotectionReperfusion InjurySpinal Cord IschemiaSuperoxide DismutaseMotor NeuronsABSTRACT Introduction: Paraplegia may develop as a result of spinal cord ischemia-reperfusion injury in patients who underwent thoracoabdominal aortic surgery. The objective of this research is to determine the neuroprotective effects of ginsenoside Rd pretreatment in a rat model of spinal cord ischemia-reperfusion injury. Methods: Sprague-Dawley rats (n=36) were randomly assigned to three groups. The sham (n=12) and control (n=12) groups received normal saline orally. The Rd group (n=12) received ginsenoside Rd (100 mg/kg) orally 48 hours before the induction of spinal cord ischemia. Spinal cord ischemia was induced by aortic occlusion using a Fogarty balloon catheter in the Rd and control groups. A neurological assessment according to the motor deficit index and a histological evaluation of the spinal cord were performed. To evaluate the antioxidant activity of ginsenoside Rd, malondialdehyde levels and superoxide dismutase activity were determined. Further, the tissue levels of tumor necrosis factor-alpha and interleukin-1 beta were measured. Results: The Rd group showed significantly lower motor deficit index scores than did the control group throughout the entire experimental period (P<0.001). The Rd group demonstrated significantly greater numbers of normal motor neurons than did the control group (P=0.039). The Rd group exhibited decreased malondialdehyde levels (P<0.001) and increased superoxide dismutase activity (P=0.029) compared to the control group. Tumor necrosis factor-alpha and interleukin-1 beta tissue levels were significantly decreased in the Rd group (P<0.001). Conclusion: Ginsenoside Rd pretreatment may be a promising treatment to prevent ischemia-reperfusion injury in patients who undergo thoracoabdominal aortic surgery.Sociedade Brasileira de Cirurgia Cardiovascular2022-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-76382022005007206Brazilian Journal of Cardiovascular Surgery n.ahead 2022reponame:Brazilian Journal of Cardiovascular Surgery (Online)instname:Sociedade Brasileira de Cirurgia Cardiovascular (SBCCV)instacron:SBCCV10.21470/1678-9741-2021-0548info:eu-repo/semantics/openAccessKim,Dong JungHan,SungheeLim,Cheongeng2022-09-15T00:00:00Zoai:scielo:S0102-76382022005007206Revistahttp://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:2022-09-15T00:00Brazilian Journal of Cardiovascular Surgery (Online) - Sociedade Brasileira de Cirurgia Cardiovascular (SBCCV)false |
dc.title.none.fl_str_mv |
The Neuroprotective Effects of Ginsenoside Rd Pretreatment in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury |
title |
The Neuroprotective Effects of Ginsenoside Rd Pretreatment in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury |
spellingShingle |
The Neuroprotective Effects of Ginsenoside Rd Pretreatment in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury Kim,Dong Jung Ginsenosides Spinal Cord Paraplegia Neuroprotection Reperfusion Injury Spinal Cord Ischemia Superoxide Dismutase Motor Neurons |
title_short |
The Neuroprotective Effects of Ginsenoside Rd Pretreatment in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury |
title_full |
The Neuroprotective Effects of Ginsenoside Rd Pretreatment in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury |
title_fullStr |
The Neuroprotective Effects of Ginsenoside Rd Pretreatment in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury |
title_full_unstemmed |
The Neuroprotective Effects of Ginsenoside Rd Pretreatment in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury |
title_sort |
The Neuroprotective Effects of Ginsenoside Rd Pretreatment in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury |
author |
Kim,Dong Jung |
author_facet |
Kim,Dong Jung Han,Sunghee Lim,Cheong |
author_role |
author |
author2 |
Han,Sunghee Lim,Cheong |
author2_role |
author author |
dc.contributor.author.fl_str_mv |
Kim,Dong Jung Han,Sunghee Lim,Cheong |
dc.subject.por.fl_str_mv |
Ginsenosides Spinal Cord Paraplegia Neuroprotection Reperfusion Injury Spinal Cord Ischemia Superoxide Dismutase Motor Neurons |
topic |
Ginsenosides Spinal Cord Paraplegia Neuroprotection Reperfusion Injury Spinal Cord Ischemia Superoxide Dismutase Motor Neurons |
description |
ABSTRACT Introduction: Paraplegia may develop as a result of spinal cord ischemia-reperfusion injury in patients who underwent thoracoabdominal aortic surgery. The objective of this research is to determine the neuroprotective effects of ginsenoside Rd pretreatment in a rat model of spinal cord ischemia-reperfusion injury. Methods: Sprague-Dawley rats (n=36) were randomly assigned to three groups. The sham (n=12) and control (n=12) groups received normal saline orally. The Rd group (n=12) received ginsenoside Rd (100 mg/kg) orally 48 hours before the induction of spinal cord ischemia. Spinal cord ischemia was induced by aortic occlusion using a Fogarty balloon catheter in the Rd and control groups. A neurological assessment according to the motor deficit index and a histological evaluation of the spinal cord were performed. To evaluate the antioxidant activity of ginsenoside Rd, malondialdehyde levels and superoxide dismutase activity were determined. Further, the tissue levels of tumor necrosis factor-alpha and interleukin-1 beta were measured. Results: The Rd group showed significantly lower motor deficit index scores than did the control group throughout the entire experimental period (P<0.001). The Rd group demonstrated significantly greater numbers of normal motor neurons than did the control group (P=0.039). The Rd group exhibited decreased malondialdehyde levels (P<0.001) and increased superoxide dismutase activity (P=0.029) compared to the control group. Tumor necrosis factor-alpha and interleukin-1 beta tissue levels were significantly decreased in the Rd group (P<0.001). Conclusion: Ginsenoside Rd pretreatment may be a promising treatment to prevent ischemia-reperfusion injury in patients who undergo thoracoabdominal aortic surgery. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-01-01 |
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=S0102-76382022005007206 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-76382022005007206 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.21470/1678-9741-2021-0548 |
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 n.ahead 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 |
_version_ |
1752126603970740224 |