Author/Authors :
Kun-Ling Tsai، نويسنده , , Yi-Hsiang Huang، نويسنده , , Chung-Lan Kao، نويسنده , , De-Ming Yang، نويسنده , , Hsin-Chen Lee، نويسنده , , Hsiang-Yun Chou، نويسنده , , Yu-Chih Chen، نويسنده , , Guang-Yuh Chiou، نويسنده , , Li-Hsin Chen، نويسنده , , Yiping Yang، نويسنده , , Tsan-Hung Chiu، نويسنده , , Chiou-Sheng Tsai، نويسنده , , Hsiu-Chung Ou، نويسنده , , Shih-Hwa Chiou، نويسنده ,
Abstract :
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.
Keywords :
Inflammation , oxLDL , CoQ10 , NO , ROS , apoptosis
