ABL Inhibits ROS Products Induced By De-endothelium And Hyperlipidemia In Rats

Objective: Reactive oxygen species (ROS) play a key role in atherosclerosis (AS) and restenosis (RS). Increased bioavailavility of vascular ROS leads to endothelial cells injury and vascular smooth muscle cells (VSMC) growth and apoptosis. Lipid peroxidations, such as malondialdehyde (MDA), products of polyunsaturated fatty acids oxidized by ROS, are of more cytotoxicity. ROS can convert low-density lipoprotein (LDL) to ox-LDL efficiently. When getting across the endothelium into the artery wall, ox-LDL is taken up by macrophages to form foam cells. ROS induced by some inflammatory cytokines can also stimulate activation of transcription factors, up-regulate chemokine production and recruit inflammatory cells, and be involved in vascular inflammation and injury. 1-o-acetylbritannilactone (ABL) extracted from Inula Britannica-F can block neointima formation through its antioxidant effects.Methods:1 Establishment of animal model: (1) Hyperlipidemia modelSD rats were randomly divided into three groups: normal group, hyperlipidemia group, and hyperlipidemia with ABL...