Role Of Oxidative Stress In Intimal Hyperplasia Lesion Induced By Vascular Adventitial Injury And Intervention Study

Vascular adventitia was involved in the initiation and progression of atherosclerosis, but the mechanism is still unclear. An animal model of vascular adventitial injury was established by combining collogenase digestion and mechanical dissection. HE staining was used to reveal morphological changes in vessels after adventitial injury, RQ-PCR to measure expression of mRNA of p22phox, subunit of NADPH oxidase, antioxidant heme oxygenase-1,ROS sensitive gene MCP-1 and PDGF, and fluorescence probe to detect ROS produced in vessels. The results showed that there were intimal hyperplasia lesions in vessels with adventitial injury but not in controls. The ration of mRNA of p22phox/HO-1, and expression of mRNA of PDGF and MCP-1 were upregulated significantly. ROS production increased significantly too, which was consistent with the change of p22phox/HO-1 ratio.Treatment with Tongxl and atorvastatin could inhibit intimal lesions and reduce the level of mRNA of p22phox. All these results leads to these conclusions: firstly, vascular adventitia is involved in the pathological process of intimal hyperplasia; secondly, oxidative stress caused by increased NADPH oxidase activity may be one of the mechanisms; the last one, Tongxl and atorvastatin alleviate intimal hyperplasia lesion by inhibition of NADPH oxidase dependent oxidative stress.