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Ocimum gratissimum Aqueous Extract Protects H9c2 Myocardiac Cells from H(2)O(2)-Induced Cell Apoptosis through Akt Signalling

Increased cell death of cardiomyocyte by oxidative stress is known to cause dysfunction of the heart. O. gratissimum is one of the more well-known medicinal plants among the Ocimum species and widely used in treatment of inflammatory diseases. In this study, we hypothesized that aqueous extract of O...

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Autores principales: Lee, Mu-Jang, Chen, Han-Min, Tzang, Bor-Show, Lin, Chiu-Wen, Wang, Chau-Jong, Liu, Jer-Yuh, Kao, Shao-Hsuan
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2952314/
https://www.ncbi.nlm.nih.gov/pubmed/20953436
http://dx.doi.org/10.1155/2011/578060
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author Lee, Mu-Jang
Chen, Han-Min
Tzang, Bor-Show
Lin, Chiu-Wen
Wang, Chau-Jong
Liu, Jer-Yuh
Kao, Shao-Hsuan
author_facet Lee, Mu-Jang
Chen, Han-Min
Tzang, Bor-Show
Lin, Chiu-Wen
Wang, Chau-Jong
Liu, Jer-Yuh
Kao, Shao-Hsuan
author_sort Lee, Mu-Jang
collection PubMed
description Increased cell death of cardiomyocyte by oxidative stress is known to cause dysfunction of the heart. O. gratissimum is one of the more well-known medicinal plants among the Ocimum species and widely used in treatment of inflammatory diseases. In this study, we hypothesized that aqueous extract of O. gratissimum leaf (OGE) may protect myocardiac cell H9c2 from oxidative injury by hydrogen peroxide (H(2)O(2)). Our results revealed that OGE pretreatment dose-dependently protects H9c2 cells from cell death when exposed to H(2)O(2). Additionally, DNA condensation induced by H(2)O(2) was also reduced by OGE pretreatment, suggesting that Ocimum gratissimum extract may attenuate H(2)O(2)-induced chromosome damage. Further investigation showed that OGE pretreatment inhibited H(2)O(2)-induced activation of caspase-3 and caspase-9, as well as H(2)O(2)-induced upregulation of proapoptotic Apaf-1 and the release of cytosolic cytochrome c, but has little effect on the activation of caspase-8. Additionally, OGE pretreatment significantly upregulated Bcl-2 expression and Akt phosphorylation, and slightly affected the phosphorylation of mitogen-activated protein kinases including p38 MAPK and JNK. Taken together, our findings revealed that Ocimum gratissimum extract effectively inhibited the mitochondrial pathway and upregulated Bcl-2 expression, which may be important in protecting H9c2 cells from H(2)O(2)-induced cell death.
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spelling pubmed-29523142010-10-15 Ocimum gratissimum Aqueous Extract Protects H9c2 Myocardiac Cells from H(2)O(2)-Induced Cell Apoptosis through Akt Signalling Lee, Mu-Jang Chen, Han-Min Tzang, Bor-Show Lin, Chiu-Wen Wang, Chau-Jong Liu, Jer-Yuh Kao, Shao-Hsuan Evid Based Complement Alternat Med Research Article Increased cell death of cardiomyocyte by oxidative stress is known to cause dysfunction of the heart. O. gratissimum is one of the more well-known medicinal plants among the Ocimum species and widely used in treatment of inflammatory diseases. In this study, we hypothesized that aqueous extract of O. gratissimum leaf (OGE) may protect myocardiac cell H9c2 from oxidative injury by hydrogen peroxide (H(2)O(2)). Our results revealed that OGE pretreatment dose-dependently protects H9c2 cells from cell death when exposed to H(2)O(2). Additionally, DNA condensation induced by H(2)O(2) was also reduced by OGE pretreatment, suggesting that Ocimum gratissimum extract may attenuate H(2)O(2)-induced chromosome damage. Further investigation showed that OGE pretreatment inhibited H(2)O(2)-induced activation of caspase-3 and caspase-9, as well as H(2)O(2)-induced upregulation of proapoptotic Apaf-1 and the release of cytosolic cytochrome c, but has little effect on the activation of caspase-8. Additionally, OGE pretreatment significantly upregulated Bcl-2 expression and Akt phosphorylation, and slightly affected the phosphorylation of mitogen-activated protein kinases including p38 MAPK and JNK. Taken together, our findings revealed that Ocimum gratissimum extract effectively inhibited the mitochondrial pathway and upregulated Bcl-2 expression, which may be important in protecting H9c2 cells from H(2)O(2)-induced cell death. Hindawi Publishing Corporation 2011 2010-08-30 /pmc/articles/PMC2952314/ /pubmed/20953436 http://dx.doi.org/10.1155/2011/578060 Text en Copyright © 2011 Mu-Jang Lee et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Lee, Mu-Jang
Chen, Han-Min
Tzang, Bor-Show
Lin, Chiu-Wen
Wang, Chau-Jong
Liu, Jer-Yuh
Kao, Shao-Hsuan
Ocimum gratissimum Aqueous Extract Protects H9c2 Myocardiac Cells from H(2)O(2)-Induced Cell Apoptosis through Akt Signalling
title Ocimum gratissimum Aqueous Extract Protects H9c2 Myocardiac Cells from H(2)O(2)-Induced Cell Apoptosis through Akt Signalling
title_full Ocimum gratissimum Aqueous Extract Protects H9c2 Myocardiac Cells from H(2)O(2)-Induced Cell Apoptosis through Akt Signalling
title_fullStr Ocimum gratissimum Aqueous Extract Protects H9c2 Myocardiac Cells from H(2)O(2)-Induced Cell Apoptosis through Akt Signalling
title_full_unstemmed Ocimum gratissimum Aqueous Extract Protects H9c2 Myocardiac Cells from H(2)O(2)-Induced Cell Apoptosis through Akt Signalling
title_short Ocimum gratissimum Aqueous Extract Protects H9c2 Myocardiac Cells from H(2)O(2)-Induced Cell Apoptosis through Akt Signalling
title_sort ocimum gratissimum aqueous extract protects h9c2 myocardiac cells from h(2)o(2)-induced cell apoptosis through akt signalling
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2952314/
https://www.ncbi.nlm.nih.gov/pubmed/20953436
http://dx.doi.org/10.1155/2011/578060
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