Fig 2.

Regulatory mechanisms of interactions between oxidative stress and inflammation. PPAR-γ reduces the expressions of ICAM-1, VCAM-1 and MCP-1, resulting in reduced macrophage accumulation, ROS production and ox-LDL deposit. In addition, PPAR-γ increases expressions of CD36 and anti-oxidant enzymes SOD and GPX, resulting in a further reduction of ox-LDL. Higher PPAR-γ is also associated with increased LXR-α and ABCA-1 expression, resulting in a decrease of cholesterol and lipids. The reduction in ox-LDL is associated with a decrease of TLR-mediated inflammation, and thereby reduced ROS production. In addition this reduction is associated with higher NOS production resulting in improved endothelial vasoreactivity, blood pressure regulation and left ventricle function. Reduction of ox-LDL results in restoring PPAR-γ expression that is associated with increased IRS-2 and glucose transporter-4 expressions, which are important regulators of insulin sensitivity and glucose uptake. Improved insulin action results in decreased mitochondrial oxidative stress, increased SOD-2 expression and reduced ROS production.