The Mechanism In The Regulation Of MiR-146a Promoted Atherosclerotic Plaque Formation

ObjectiveTo study the effect of mi R-146 a in atherosclerotic plaque and the mechanism.MethodsApplicated the lymphocyte separation technology to separate the peripheral blood lymphocytes of rat, and induced it to mononuclear marcrophages. Used mi R-146 a mimic and mi R-146 a inhibitor to transfect peripheral blood mononuclear macrophage of rat, and made the macrophages bubblization after the successful transfection. Analyzed the impact of mi R-146 a on lipid build up in cells by used oil red O staining and lipid dyeing semi-quantitative. Western blot detected the expression of CEH, ABCA1 and ABCG1, analyzed the relationship between mi R-146 a and CEH and the impacted of mi R-146 a on reverse cholesterol transport.ResultsThe grey value analysis of Western blot test show that the CEH expression in mi R-146 a mimic transfection group is less than the control group, which means mi R-146 a content elevated could inhibit the expression of CEH. And the expression of ABCA1 and ABCA1 in mi R-146 a inhibitor transfection group is more than in mi R-146 a mimic transfection group, thus we believe that mi R-146 a can inhibit the expression of ATP-blinding cassetle transporter ABCA1 and ABCG1 which associated with cholesterol outflow. Oil red O staining showed that the cells in mi R-146 a inhibitor transfection compared with control group are mostly oval or irregular in shape. Oil red staining positive cells decreased significantly, nuclei stained blue, cytoplasm red dye is not obvious. The ratio of positive cells in mi R-146 a mimic transfection group, the blank group and mi R-146 a inhibitor transfection group are 82.1﹪±3.1﹪, 73.2﹪±0.16﹪ and 16.25﹪±2.1﹪.Conclusionsmi R-146 a can inhibit the expression of CEH in the rat peripheral blood mononuclear macrophage, meanwhile make the cell surface channel proteins increase, such as ABCA1 and ABCG1.Promote the progress of RCT in varying degrees and hinder the free outflow of cholesterol, lead to the formation of atherosclerotic plaques eventually.