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Gastrodin ameliorates subacute phase cerebral ischemia-reperfusion injury by inhibiting inflammation and apoptosis in rats

Gastrodin (GAS), which is extracted from the Chinese herbal medicine Gastrodia elata Blume, has long been used to improve stroke, epilepsy, dizziness and dementia. However, the effects and underlying mechanisms of GAS on subacute phase cerebral ischemia-reperfusion (I/R) injury remain unknown. The a...

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Autores principales: Liu, Bo, Li, Fei, Shi, Jingshan, Yang, Danli, Deng, Yuanyuan, Gong, Qihai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5101922/
https://www.ncbi.nlm.nih.gov/pubmed/27748849
http://dx.doi.org/10.3892/mmr.2016.5785
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author Liu, Bo
Li, Fei
Shi, Jingshan
Yang, Danli
Deng, Yuanyuan
Gong, Qihai
author_facet Liu, Bo
Li, Fei
Shi, Jingshan
Yang, Danli
Deng, Yuanyuan
Gong, Qihai
author_sort Liu, Bo
collection PubMed
description Gastrodin (GAS), which is extracted from the Chinese herbal medicine Gastrodia elata Blume, has long been used to improve stroke, epilepsy, dizziness and dementia. However, the effects and underlying mechanisms of GAS on subacute phase cerebral ischemia-reperfusion (I/R) injury remain unknown. The aim of the present study was to investigate the effects and mechanisms of GAS on cerebral I/R injury in rats. The rats were pretreated with GAS by gavage for 7 days followed by I/R surgery, and were then treated with GAS for 7 days after I/R surgery. Neurological deficits were assessed on days 1, 3 and 7 post-cerebral I/R injury. 2,3,5-Triphenyltetrazolium chloride staining was using to measure the infarct volume; morphological alterations were observed by hematoxylin and eosin staining under an optical microscope; apoptosis in the hippocampus and cortex was observed by terminal deoxynucleotidyl transferase dUTP nick end labeling staining; and the level of mRNA and protein expression was tested by reverse transcription-quantitative polymerase chain reation and western blot analysis, respectively. GAS markedly attenuated I/R-induced disability and histological damage, alleviated neuronal apoptosis, and reduced the mRNA and protein expression levels of inflammatory and proapoptotic factors, including interleukin-1β, cyclooxygenase-2, inducible nitric oxide synthase and cleaved caspase-3. These findings suggested that GAS may ameliorate subacute phase cerebral I/R injury by inhibiting inflammation and apoptosis in rats; therefore, GAS may be considered a potential candidate for the treatment of cerebral ischemia.
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spelling pubmed-51019222016-11-22 Gastrodin ameliorates subacute phase cerebral ischemia-reperfusion injury by inhibiting inflammation and apoptosis in rats Liu, Bo Li, Fei Shi, Jingshan Yang, Danli Deng, Yuanyuan Gong, Qihai Mol Med Rep Articles Gastrodin (GAS), which is extracted from the Chinese herbal medicine Gastrodia elata Blume, has long been used to improve stroke, epilepsy, dizziness and dementia. However, the effects and underlying mechanisms of GAS on subacute phase cerebral ischemia-reperfusion (I/R) injury remain unknown. The aim of the present study was to investigate the effects and mechanisms of GAS on cerebral I/R injury in rats. The rats were pretreated with GAS by gavage for 7 days followed by I/R surgery, and were then treated with GAS for 7 days after I/R surgery. Neurological deficits were assessed on days 1, 3 and 7 post-cerebral I/R injury. 2,3,5-Triphenyltetrazolium chloride staining was using to measure the infarct volume; morphological alterations were observed by hematoxylin and eosin staining under an optical microscope; apoptosis in the hippocampus and cortex was observed by terminal deoxynucleotidyl transferase dUTP nick end labeling staining; and the level of mRNA and protein expression was tested by reverse transcription-quantitative polymerase chain reation and western blot analysis, respectively. GAS markedly attenuated I/R-induced disability and histological damage, alleviated neuronal apoptosis, and reduced the mRNA and protein expression levels of inflammatory and proapoptotic factors, including interleukin-1β, cyclooxygenase-2, inducible nitric oxide synthase and cleaved caspase-3. These findings suggested that GAS may ameliorate subacute phase cerebral I/R injury by inhibiting inflammation and apoptosis in rats; therefore, GAS may be considered a potential candidate for the treatment of cerebral ischemia. D.A. Spandidos 2016-11 2016-09-26 /pmc/articles/PMC5101922/ /pubmed/27748849 http://dx.doi.org/10.3892/mmr.2016.5785 Text en Copyright: © Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Liu, Bo
Li, Fei
Shi, Jingshan
Yang, Danli
Deng, Yuanyuan
Gong, Qihai
Gastrodin ameliorates subacute phase cerebral ischemia-reperfusion injury by inhibiting inflammation and apoptosis in rats
title Gastrodin ameliorates subacute phase cerebral ischemia-reperfusion injury by inhibiting inflammation and apoptosis in rats
title_full Gastrodin ameliorates subacute phase cerebral ischemia-reperfusion injury by inhibiting inflammation and apoptosis in rats
title_fullStr Gastrodin ameliorates subacute phase cerebral ischemia-reperfusion injury by inhibiting inflammation and apoptosis in rats
title_full_unstemmed Gastrodin ameliorates subacute phase cerebral ischemia-reperfusion injury by inhibiting inflammation and apoptosis in rats
title_short Gastrodin ameliorates subacute phase cerebral ischemia-reperfusion injury by inhibiting inflammation and apoptosis in rats
title_sort gastrodin ameliorates subacute phase cerebral ischemia-reperfusion injury by inhibiting inflammation and apoptosis in rats
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5101922/
https://www.ncbi.nlm.nih.gov/pubmed/27748849
http://dx.doi.org/10.3892/mmr.2016.5785
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