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Allicin prevents H(2)O(2)-induced apoptosis of HUVECs by inhibiting an oxidative stress pathway

BACKGROUND: Allicin, a primary ingredient of garlic, has been proposed to possess cardioprotective properties, which are commonly mediated by improved endothelial function. METHODS: To investigate the effect and mechanism of allicin on the apoptosis of human umbilical vein endothelial cells (HUVECs)...

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Autores principales: Chen, Sisi, Tang, Yuye, Qian, Ying, Chen, Ruyi, Zhang, Lin, Wo, Like, Chai, Hui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4158076/
https://www.ncbi.nlm.nih.gov/pubmed/25174844
http://dx.doi.org/10.1186/1472-6882-14-321
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author Chen, Sisi
Tang, Yuye
Qian, Ying
Chen, Ruyi
Zhang, Lin
Wo, Like
Chai, Hui
author_facet Chen, Sisi
Tang, Yuye
Qian, Ying
Chen, Ruyi
Zhang, Lin
Wo, Like
Chai, Hui
author_sort Chen, Sisi
collection PubMed
description BACKGROUND: Allicin, a primary ingredient of garlic, has been proposed to possess cardioprotective properties, which are commonly mediated by improved endothelial function. METHODS: To investigate the effect and mechanism of allicin on the apoptosis of human umbilical vein endothelial cells (HUVECs), we used Propidium iodide (PI) staining and Annexin V/ PI staining assays to establish a model of oxidative stress apoptosis induced by H(2)O(2). MTT, RT-PCR and western-blot assays were used to detect the effects and mechanism of allicin on the model. RESULTS: PI staining, Annexin V/ PI staining assays and morphological assessment suggest that the cell death induced by 0.5 mM H(2)O(2) is primarily apoptotic. Conversely, allicin reverses the effect of H(2)O(2) on cell death, suggesting a role in protecting HUVECs from apoptosis. We demonstrated that H(2)O(2) activates PARP cleavage, reduces pro-Caspase-3 levels and activates Bax expression; however, allicin inhibits each of these apoptotic signaling indicators. Allicin also reduces the levels of malondialdehyde and increases the levels of superoxide dismutase, nitric oxide release and endothelial nitric oxide synthase mRNA, but has no significant effect on inducible nitric oxide synthase mRNA levels. CONCLUSION: These results demonstrate that allicin has powerful effects in protecting HUVECs from apoptosis and suggest that protection occurs via a mechanism involving the protection from H(2)O(2)-mediated oxidative stress.
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spelling pubmed-41580762014-09-10 Allicin prevents H(2)O(2)-induced apoptosis of HUVECs by inhibiting an oxidative stress pathway Chen, Sisi Tang, Yuye Qian, Ying Chen, Ruyi Zhang, Lin Wo, Like Chai, Hui BMC Complement Altern Med Research Article BACKGROUND: Allicin, a primary ingredient of garlic, has been proposed to possess cardioprotective properties, which are commonly mediated by improved endothelial function. METHODS: To investigate the effect and mechanism of allicin on the apoptosis of human umbilical vein endothelial cells (HUVECs), we used Propidium iodide (PI) staining and Annexin V/ PI staining assays to establish a model of oxidative stress apoptosis induced by H(2)O(2). MTT, RT-PCR and western-blot assays were used to detect the effects and mechanism of allicin on the model. RESULTS: PI staining, Annexin V/ PI staining assays and morphological assessment suggest that the cell death induced by 0.5 mM H(2)O(2) is primarily apoptotic. Conversely, allicin reverses the effect of H(2)O(2) on cell death, suggesting a role in protecting HUVECs from apoptosis. We demonstrated that H(2)O(2) activates PARP cleavage, reduces pro-Caspase-3 levels and activates Bax expression; however, allicin inhibits each of these apoptotic signaling indicators. Allicin also reduces the levels of malondialdehyde and increases the levels of superoxide dismutase, nitric oxide release and endothelial nitric oxide synthase mRNA, but has no significant effect on inducible nitric oxide synthase mRNA levels. CONCLUSION: These results demonstrate that allicin has powerful effects in protecting HUVECs from apoptosis and suggest that protection occurs via a mechanism involving the protection from H(2)O(2)-mediated oxidative stress. BioMed Central 2014-08-30 /pmc/articles/PMC4158076/ /pubmed/25174844 http://dx.doi.org/10.1186/1472-6882-14-321 Text en © Chen et al.; licensee BioMed Central Ltd. 2014 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Chen, Sisi
Tang, Yuye
Qian, Ying
Chen, Ruyi
Zhang, Lin
Wo, Like
Chai, Hui
Allicin prevents H(2)O(2)-induced apoptosis of HUVECs by inhibiting an oxidative stress pathway
title Allicin prevents H(2)O(2)-induced apoptosis of HUVECs by inhibiting an oxidative stress pathway
title_full Allicin prevents H(2)O(2)-induced apoptosis of HUVECs by inhibiting an oxidative stress pathway
title_fullStr Allicin prevents H(2)O(2)-induced apoptosis of HUVECs by inhibiting an oxidative stress pathway
title_full_unstemmed Allicin prevents H(2)O(2)-induced apoptosis of HUVECs by inhibiting an oxidative stress pathway
title_short Allicin prevents H(2)O(2)-induced apoptosis of HUVECs by inhibiting an oxidative stress pathway
title_sort allicin prevents h(2)o(2)-induced apoptosis of huvecs by inhibiting an oxidative stress pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4158076/
https://www.ncbi.nlm.nih.gov/pubmed/25174844
http://dx.doi.org/10.1186/1472-6882-14-321
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