Format

Send to

Choose Destination
Chem Biol Interact. 2015 Feb 25;228:35-45. doi: 10.1016/j.cbi.2015.01.007. Epub 2015 Jan 17.

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

Author information

1
Department of Internal Medicine, Chung Shan Medical University Hospital, No. 110, Section 1, Jianguo N. Road, Taichung, Taiwan; Institute of Medicine, Chung Shan Medical University, No. 110, Section 1, Jianguo N. Road, Taichung, Taiwan.
2
Clinical Laboratory, Chung Shan Medical University Hospital, No. 110, Section 1, Jianguo N. Road, Taichung, Taiwan; Institute of Biochemistry and Biotechnology, Chung Shan Medical University, No. 110, Section 1, Jianguo N. Road, Taichung, Taiwan.
3
Institute of Biochemistry and Biotechnology, Chung Shan Medical University, No. 110, Section 1, Jianguo N. Road, Taichung, Taiwan.
4
Institute and Department of Food Science, Central Taiwan University of Science and Technology, No. 11 Pu-tzu Lane, Pu-tzu Road, Taichung 406, Taiwan. Electronic address: scchu@ctust.edu.tw.

Abstract

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.

KEYWORDS:

Apoptosis; Atherosclerosis; Capsaicin; HUVECs; OxLDL

PMID:
25603234
DOI:
10.1016/j.cbi.2015.01.007
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center