Allicin prevents oxidized low-density lipoprotein-induced endothelial cell injury by inhibiting apoptosis and oxidative stress pathway. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Chen, Xiaoshu; Pang, Sunian; Lin, Jianfeng; Xia, Jianlan; Wang, Yi
• Is Part Of: BMC complementary and alternative medicine. Volume 16:Issue 1(2016)
• Page Start: 1
• Page End: 6
• Publication Date: 2016-12
• Subjects: Allicin -- Oxidized low-density lipoprotein -- Endothelial cell -- Apoptosis -- Oxidative stress; Alternative medicine -- Periodicals; Complementary Therapies -- Periodicals; 615.505
• DOI: 10.1186/s12906-016-1126-9
• Languages: English
• ISSNs: 1472-6882

Abstract

Abstract Background Vascular endothelial apoptosis is significantly associated with atherosclerosis and cardiovascular diseases, for which oxidized low-density lipoprotein (ox-LDL) is a major risk factor. Allicin, the primary active ingredient of garlic, has been found to have cardiovascular protective effect by changing the fatty-acid composition, but its effect on ox-LDL-induced vascular endothelial injury remains unclear. We investigated the protective effect of allicin on cell viability, LDH release, apoptosis and apoptotic signaling in human umbilical vein endothelial cells (HUVECs). Methods In cultured HUVEC cell line, ox-LDL induced injury was investigated. The cell viability and injury were evaluated by using cell proliferation Assay kit and LDH release assay. The apoptosis was evaluated by the Annexin V-FITC kit. The activity of caspase-3 was assessed using a colorimetric caspase-3 assay kit. The ROS production was evaluated by fluorometric assay and NADPH oxidase activity was assessed with a GENMED kit. Results Exposure of HUVECs to ox-LDL (150 μg/ml) reduced cell viability, induced apoptosis and increased activity of caspase-3, NADPH oxidase, and reactive oxygen species (ROS) production. The pretreatment with allicin (30 and 100 μM) significantly rescued the cell viability, inhibited ox-LDL-induced apoptosis and activity of caspase-3, NADPH oxidase and ROS production in HUVECs, and the protective effect is concentration-dependent. The allicin (100 μM) alone did not show significant difference from control. Our study demonstrated that allicin protected HUVECs from ox-LDL-induced endothelial injury by reducing the apoptosis, mediated by inhibition of caspase-3 and NADPH oxidase related apoptotic signaling. Conclusions Allicin prevents ox-LDL-induced endothelial cell injury by inhibiting apoptosis and oxidative stress pathway.