The Experimental Study Of The Effects Of Oxidized Low-density Lipoprotein And Vitamin C On The Stability Of Atherosclerotic Plaque

Background Atherosclerotic plaque rupture, haemorrhage and thrombosis in the coronary arteries can lead to the acute coronary syndrome, including unstable angina, acute myocardial infarction and sudden death. Unstable plaque which is vulnerable and prone to rupture has a thin fibrous cap with reduced extracellular matrix. The extracellular matrix in atherosclerotic plaque is produced by vascular smooth muscle cells. Vascular smooth muscle cells can also produce matrix metalloproteinases(MMPs) and tissue inhibitor of metalloproteinases (TIMPs). Vascular smooth muscle cells play an important role in the formation, progression and deterioration of atherosclerosis.Objective There is a great deal of oxidized low-density lipoprotein(ox-LDL) in atherosclerotic plaque. Ox-LDL causes atherosclerosis by injuring endothelial cells, accelerating formation of foam cells, attracting leukocytes infiltration and inducing smooth muscle cells proliferation. Many studies indicate that ox-LDL also plays an important role in plaque rupture. The mechanism of ox-LDL causing plaque rupture is not clear up to now yet. This research work studied the effect of ox-LDL and vitamin C on the expression of type I and III procollagen gene, synthesis and activity of MMPs/TIMPs and the apoptosis of vascular smooth muscle cells. By exploring the mechanism of plaque rupture, we attempted to provide new clues for prevention and treatment of acute coronary syndrome.Method This basic experiment was based on the human fetal aortic vascular smooth muscle cells culture. Human vascular smooth muscle cells were incubated with ox-LDL, n-LDL and vitamin C. The techniques of Northern blot analysis , quantitative RT-PCR, Western blot analysis, gelatin SDS-PAGE zymography and measure of breaks of...