Effect of C-reactive protein and Oxidized Low Density Lipoprotein on superoxide production from Human Aortic Endothelial Cells

• Main Authors: Ya-shinan Yang, 楊亞璇
• Other Authors: Kuang-tse Huang
• Format: Others
• Language: zh-TW
• Published: 2006
• Online Access: http://ndltd.ncl.edu.tw/handle/78464789642246843673

碩士 === 國立中正大學 === 化學工程所 === 94 === Atherosclerosis generally accepted as a chronic low-grade inflammatory disease leads to the thickening, hardening, and loss of elasticity of arterial wall. Recent investigations show that oxidized low density lipoprotein (oxLDL) and C-reactive protein (CRP) play an important role in atherosclerosis. CRP and oxLDL have been shown to increase intracellular superoxide (O2-) production. However, which enzyme system involves in the CRP- and oxLDL-induced O2- production remains unknown. Here, we investigated the effect of oxLDL and CRP on the intracellular O2- production in the presence and absence of the commonly used superoxide dismutase (SOD) inhibitor (diethyldithiocarbamate; DETC), NAD(P)H oxidase inhibitor (apocynin), endothelial nitric oxide synthase (eNOS) inhibitors (L-NG-Nitroarginine (L-NNA) and L-NG-Nitroarginine methyl ester (L-NAME)), and mitochondrial respiration inhibitors (myxothiazol and rotenone). Notably, DETC not only inhibits SOD but also xanthine oxidase. Our results show that the contribution of the basal O2- production from various sources is NAD(P)H oxidase. The level of intracellular O2- is increased by a CRP concentration of 1 mg/mL, but decreases with higher concentrations of CRP. The source of intracellular O2- production seems also mainly from NAD(P)H oxidase. On the other hand, oxLDL increases intracellular O2- production in a dose dependent manner and the oxLDL-induced O2- production may involve xanthine oxidase, NAD(P)H oxidase, and mitochondrial respiration. In addition, the oxLDL/CRPcomplex affects the O2- production from xanthine oxidase and NAD(P)H oxidase.