Buyang Huanwu Decoction attenuates H2O2-induced apoptosis by inhibiting reactive oxygen species-mediated mitochondrial dysfunction pathway in human umbilical vein endothelial cells

BMC Complementary and Alternative Medicine

Research Article

Xiaoxing Xiong¹  Yu Zhu²  Hao Jiang²  Kaiyuan Huang²  Renya Zhan²  Jianwei Pan²  Jian Shen²  Chengzhang Shi² 

[1] Department of Anesthesiology, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, People’s Republic of China;Department of Neurosurgery, First Affiliated Hospital, School of Medicine, Zhejiang University, No. 79 Qingchun Road, Hangzhou, Zhejiang, People’s Republic of China;

关键词: Buyang Huanwu Decoction;    Reactive oxygen species;    Apoptosis;    Ritochondria;    Cerebral ischeima;   

DOI  :  10.1186/s12906-016-1152-7

 received in 2016-02-09, accepted in 2016-05-27,  发布年份 2016

来源: Springer

【 摘 要 】

BackgroundApoptosis of endothelial cells caused by reactive oxygen species plays an important role in ischemia/reperfusion injury after cerebral infarction. Buyang Huanwu Decoction (BYHWD) has been used to treat stroke and stroke-induced disability, however, the mechanism for this treatment remains unknown. In this study, we investigated whether BYHWD can protect human umbilical vein endothelial cells (HUVECs) from H2O2-induced apoptosis and explored the underlying mechanisms.MethodsTo investigate the effect of BYHWD on the apoptosis of HUVECs, we established a H2O2-induced oxidative stress model and detected apoptosis by Hoechst 33342 and propidium iodide staining. JC-1 and DCFH-DA assays,western blotting and electron microscopy were used to examine the mechanism of BYHWD on apoptosis.ResultsPretreatment with BYHWD significantly inhibited H2O2-induced apoptosis and protein caspase-3 expression in a concentration-dependent manner. In addition, BYHWD reduced reactive oxygen species production and promoted endogenous antioxidant defenses. Furthermore, loss of mitochondrial membrane potential and structural disruption of mitochondria were both rescued by BYHWD.ConclusionsBYHWD protects HUVECs from H2O2-induced apoptosis by inhibiting oxidative stress damage and mitochondrial dysfunction. These findings indicate that BYHWD is a promising treatment for cerebral ischemia diseases.

【 授权许可】

CC BY   
© The Author(s). 2016