Capsaicin protects endothelial cells and macrophage against oxidized low-density lipoprotein-induced injury by direct antioxidant action

• Published in: Chemico-biological interactions Vol. 228; pp. 35 - 45
• Main Authors: Chen, Kuo-Shuen, Chen, Pei-Ni, Hsieh, Yih-Shou, Lin, Chin-Yin, Lee, Yi-Hsun, Chu, Shu-Chen
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 25.02.2015
• Subjects: Antioxidants - chemistry; Antioxidants - pharmacology; Apoptosis; Atherosclerosis; Capsaicin; Capsaicin - chemistry; Capsaicin - pharmacology; Cell Cycle - drug effects; Cell Death - drug effects; Cells, Cultured; Dose-Response Relationship, Drug; Human Umbilical Vein Endothelial Cells - drug effects; Human Umbilical Vein Endothelial Cells - metabolism; Humans; HUVECs; Lipoproteins, LDL - antagonists & inhibitors; Lipoproteins, LDL - chemistry; Lipoproteins, LDL - pharmacology; Macrophages - drug effects; Macrophages - metabolism; Oxidation-Reduction - drug effects; OxLDL; Structure-Activity Relationship; LDL; Capsaicin; ROS; Atherosclerosis; DAPI; TBARS; OxLDL; REM; HUVECs; Apoptosis
• ISSN: 0009-2797; 1872-7786
• DOI: 10.1016/j.cbi.2015.01.007

[Display omitted] •Capsaicin inhibited copper-induced lipid peroxidation of LDL.•Capsaicin prevented oxLDL-induced cellular dysfunction of HUVECs.•Capsaicin protected oxLDL-induced ROS generation in HUVECs.•Capsaicin reverted oxLDL-induced alterations in mitochondrial transmembrane permeability and apoptotic proteins expression.•Capsaicin blocked foam cell formation in macrophage RAW 264.7 cells. Atherosclerosis is a chronic inflammatory vascular disease. It is characterized by endothelial dysfunction, lipid accumulation, leukocyte activation, and the production of inflammatory mediators and reactive oxygen species (ROS). Capsaicin, a biologically active compound of the red pepper and chili pepper, has several anti-oxidant, anti-inflammatory, anti-cancer, and hypolipidemic biological effects. However, its protective effects on foam cell formation and endothelial injury induced by oxidized low-density lipoprotein (oxLDL) remain unclear. In this study, we evaluated the anti-oxidative activity of capsaicin, and determined the mechanism by which capsaicin rescues human umbilical vein endothelial cells (HUVECs) from oxLDL-mediated dysfunction. The anti-oxidative activity of capsaicin was defined by Apo B fragmentation and conjugated diene production of the copper-mediated oxidation of LDL. Capsaicin repressed ROS generation, as well as subsequent mitochondrial membrane potential collapse, cytochrome c expression, chromosome condensation, and caspase-3 activation induced by oxLDL in HUVECs. Capsaicin also protected foam cell formation in macrophage RAW 264.7 cells. Our results suggest that capsaicin may prevent oxLDL-induced cellular dysfunction and protect RAW 264.7 cells from LDL oxidation.