Buyang Huanwu Decoction attenuates H2O2-induced apoptosis by inhibiting reactive oxygen species-mediated mitochondrial dysfunction pathway in human umbilical vein endothelial cells. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Shen, Jian; Zhu, Yu; Huang, Kaiyuan; Jiang, Hao; Shi, Chengzhang; Xiong, Xiaoxing; Zhan, Renya; Pan, Jianwei
• Is Part Of: BMC complementary and alternative medicine. Volume 16:Issue 1(2016)
• Page Start: 1
• Page End: 11
• Publication Date: 2016-12
• Subjects: Buyang Huanwu Decoction -- Reactive oxygen species -- Apoptosis -- Ritochondria -- Cerebral ischeima; Alternative medicine -- Periodicals; Complementary Therapies -- Periodicals; 615.505
• DOI: 10.1186/s12906-016-1152-7
• Languages: English
• ISSNs: 1472-6882

Abstract

Abstract Background Apoptosis 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 H2 O2 -induced apoptosis and explored the underlying mechanisms. Methods To investigate the effect of BYHWD on the apoptosis of HUVECs, we established a H2 O2 -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. Results Pretreatment with BYHWD significantly inhibited H2 O2 -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. Conclusions BYHWD protects HUVECs from H2 O2 -induced apoptosis by inhibiting oxidative stress damage and mitochondrial dysfunction. These findings indicate that BYHWD is a promising treatment for cerebral ischemia diseases.