Allicin prevents H2O2-induced apoptosis of HUVECs by inhibiting an oxidative stress pathway

BMC Complementary and Alternative Medicine

Research Article

Hui Chai¹  Ruyi Chen¹  Lin Zhang¹  Sisi Chen¹  Ying Qian¹  Yuye Tang²  Like Wo³ 

[1] College of Life Science, Zhejiang Chinese Medical University, 310053, Hangzhou, China;Hangzhou pharmavaxin co., LTD, 310052, Hangzhou, China;The First Affiliated Hospital of Zhejiang Chinese Medicine University, 310006, Hangzhou, China;

关键词: Allicin;    Human umbilical vein endothelial cell (HUVEC);    Anti-apoptosis;    HO;   

DOI  :  10.1186/1472-6882-14-321

 received in 2014-07-17, accepted in 2014-08-27,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundAllicin, a primary ingredient of garlic, has been proposed to possess cardioprotective properties, which are commonly mediated by improved endothelial function.MethodsTo 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 H2O2. MTT, RT-PCR and western-blot assays were used to detect the effects and mechanism of allicin on the model.ResultsPI staining, Annexin V/ PI staining assays and morphological assessment suggest that the cell death induced by 0.5 mM H2O2 is primarily apoptotic. Conversely, allicin reverses the effect of H2O2 on cell death, suggesting a role in protecting HUVECs from apoptosis. We demonstrated that H2O2 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.ConclusionThese results demonstrate that allicin has powerful effects in protecting HUVECs from apoptosis and suggest that protection occurs via a mechanism involving the protection from H2O2-mediated oxidative stress.

【 授权许可】

Unknown   
© 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.