A novel mechanism of coenzyme Q10 protects against human endothelial cells from oxidative stress-induced injury by modulating NO-related pathways

伊诺斯 促炎细胞因子 一氧化氮 氧化应激 辅酶Q10 脐静脉 化学 一氧化氮合酶 活性氧 内皮干细胞 人脐静脉内皮细胞 细胞生物学 一氧化氮合酶Ⅲ型 炎症 生物化学 药理学 生物 免疫学 体外 有机化学
作者
Kun Ling Tsai,Yi Hsiang Huang,Chung Lan Kao,De Ming Yang,Hsin Chen Lee,Hsiang Chou,Yu‐Chih Chen,Guang Yuh Chiou,Li Hsin Chen,Yi Yang,Te-Fa Chiu,Chiou Sheng Tsai,Hsiu Chung Ou,Shih Hwa Chiou
出处
期刊:Journal of Nutritional Biochemistry [Elsevier BV]
卷期号:23 (5): 458-468 被引量:109
标识
DOI:10.1016/j.jnutbio.2011.01.011
摘要

Atherosclerosis is a chronic inflammatory disease of the vessel wall associated with oxidized low-density lipoprotein (oxLDL)-induced apoptosis of endothelial cells. Coenzyme Q10 (CoQ10), 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. In this study, primary human umbilical vein endothelial cell cultures treated with oxLDL were used to explore the protective effects of CoQ10. Our results showed that CoQ10 attenuated the oxLDL-induced generation of reactive oxygen species and improved the antioxidant capacity. CoQ10 also attenuated the oxLDL-mediated down-regulation of endothelial nitric oxide synthase (eNOS) and up-regulation of inducible nitric oxide synthase (iNOS). In addition, CoQ10 suppressed oxLDL-activated NF-κB and downstream inflammatory mediators, including expression of adhesion molecules, release of proinflammatory cytokines and the adherence of monocytic THP-1 cells. Moreover, CoQ10 attenuated oxLDL-altered proapoptotic responses. The inhibitor of eNOS (l-NIO 10 μM) and iNOS (1400W 10 μM) as well as NO enhancer (SNP 10 μM) were used to clean up the mechanism. These results provide new insight into the possible molecular mechanisms by which CoQ10 protects against atherogenesis by NO-related pathways.
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