Study On Actions Of C-reactive Proteinin Atherosclerosis

Cardiovascular disease?CVD?is the leading cause of death worldwide.According to global diseases study,the number of CVD deaths in 1990 was 12.3million,but now the number of CVD deaths has increased significantly to more than17.9 million.Because of its high mortality and morbidity,the prediction and treatment of cardiovascular disease is particularly important.Atherosclerosis?AS?,as the main cause of high mortality from CVD,is the pathological basis of many cardiovascular diseases,including peripheral vascular disease,cerebral infarction and coronary heart disease.Atherosclerosis is a chronic inflammatory disease,and the pathological process is mainly manifested as endothelial cell activation,mononuclear cell adhesion and migration,foam cell accumulation,atherosclerosis plaque formation,plaque rupture,thrombosis and so on.C-reactive protein?CRP?,as an acute reactive protein,is a highly sensitive marker of inflammation and tissue damage,and is closely related to the risk and prognosis of CVD.Previous research has shown that CRP has been shown to be a predictor of inflammation in AS.However,research in recent years has found that CRP may not only be a predictor,but may also be directly involved in the occurrence and development of AS.Therefore,there is fierce controversy about whether and how CRP functions in AS.This experiment explores the role and mechanism of CRP and AS in cell experiments and animal experiments.In the cell experiment,there was no difference in the number and morphology of cells between Wild-type?WT?mice and systemic knock-out CRP(CRP^-/-)mice in the extraction experiment of peritoneal macrophages,indicating that CRP did not affect the number and morphology of peritoneal macrophages in mice.The two cells were stimulated by lipopolysaccharide?LPS?and the expression levels of inflammatory factors were detected.The expression of TNFa and COX-2 was statistically different.The mRNA level of CRP^-/-mice was significantly lower than that of WT mice,indicating endogenous CRP may affect the expression level of inflammatory factors.Later,CRP was added exogenously to peritoneal macrophages to further explore the response of exogenous CRP to inflammatory factors.The results showed that the addition of exogenous CRP did not affect the inflammatory response of peritoneal macrophages.On the other hand,considering the low content of CRP in macrophages,it may be that the ability of CRP to resist infection is different,leaving the cells in a low-inflammatory state.The absence of CRP may cause peritoneal macrophages to be insensitive to LPS stimulation.Therefore,CRP may indirectly affect the inflammatory response of peritoneal macrophages.In animal experiments,ApoE^-/-and CRP^-/-ApoE^-/-mice were fed with high-fat diet to induce atherosclerosis models.Serial sections of aortic roots were analyzed by HE,Oil red O,macrophage immunohistochemical staining and aortic tree Oil red O staining.Plaque accumulation was observed in HE staining of the aortic root;Oil red O staining results showed that the plaque area of CRP^-/-ApoE^-/-mice was less than ApoE^-/-mice;Immunohistochemical staining of macrophages showed that ApoE^-/-mice had more macrophage aggregation.The aortic tree Oil red O staining results showed that the atherosclerotic plaque area of CRP^-/-ApoE^-/-mice was significantly reduced.Therefore,CRP can promote atherosclerotic lesions,increase lipid accumulation and macrophage aggregation in plaques,and further affect the formation of atherosclerotic plaques.In addition,this experiment also discussed the role of CRP and fatty liver and acute injury.CRP can aggravate the degree of fatty liver disease,reduce the lesion of acute injury,and have a protective effect on acute injury.