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A novel mechanism of Coenzyme Q10 protects against human endothelial cells from oxidative stress‐induced by modulating NO‐related pathways
Author(s) -
Tsai KunLing,
Chiou ShihHwa
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.lb454
Subject(s) - coenzyme q10 , enos , oxidative stress , chemistry , nitric oxide , umbilical vein , human umbilical vein endothelial cell , microbiology and biotechnology , apoptosis , endothelial stem cell , nitric oxide synthase , antioxidant , cell adhesion molecule , pharmacology , biochemistry , biology , in vitro , organic chemistry
Background Atherosclerosis is a chronic inflammatory disease of the vessel wall associated with oxidized low‐density lipoprotein (oxLDL)‐induced apoptosis of endothelial cells. Coenzyme Q10 (Co Q10), a potent antioxidant and a critical intermediate of the electron transport chain, has been reported to inhibit LDL oxidation and thus the progression of atherosclerosis. However, its molecular mechanisms on endothelial cells remain still unclarified. Methods In this study, primary human umbilical vein endothelial cell cultures (HUVECs) treated with oxLDL were used to explore the protective effects of Co Q10. Results Our results showed that Co Q10 attenuated the oxLDL‐induced generation of ROS and improved the antioxidant capacity. Co Q10 also attenuated the oxLDL‐mediated down‐regulation of endothelial nitric oxide synthase (eNOS) and up‐regulation of inducible nitric oxide synthase (iNOS). In addition, Co Q10 suppressed oxLDL‐activated NF‐κB and downstream inflammatory mediators, including expression of adhesion molecules, release of pro‐inflammatory cytokines, and the adherence of monocytic THP‐1 cells. Moreover, Co Q10 attenuated oxLDL‐altered pro‐apoptotic responses. The inhibitor of eNOS and iNOS as well as NO enhancer were used to clean up the mechanism involved in the protective effects. Conclusion These results provide new insight into the possible molecular mechanisms by which Co Q10 protects against atherogenesis by NO‐related pathways.