Effect Of Atorvastatin On Nox4 Expression In Atherosclerotic Plaques Of Mice

BackgroundWith the development of this medical treatment,percutaneous coronary intervention?PCI?has become a very important means for the treatment of cardiovascular diseases.However,the restenosis?RS?of damaged vascular sites after intervention and plaque rupture and bleeding still restrict the progress of this technique."China cardiovascular disease report 2016"is published.At present,the incidence and mortality of cardiovascular disease in China are still in the rising stage,and the number of cardiovascular diseases is estimated to be 290 million,including 11 million of coronary heart disease and 4 million 500 thousand of heart failure.The death of cardiovascular disease accounts for the first cause of the total death of urban and rural residents,of which the restenosis after PCI and acute cardiovascular events threaten the people's health seriously..How to effectively prevent restenosis after PCI and the occurrence of acute cardiovascular events are of great significance.The study shows that the mechanism of vascular restenosis after PCI may be caused by balloon dilatation and vascular stent implantation,causing vascular endothelial cell damage,causing local microenvironment changes,causing the proliferation and migration of macrophages and smooth muscle cells,and then forming atherosclerotic plaque?AS?.In the formation mechanism of AS,the oxidation theory provides us with an important basis.ROS is produced by the NADPH oxidase NOX protein family.It can maintain normal physiological activities of the cells.In the case of less ROS production,it has the function of immune defense,and a large number of ROX can lead to excessive oxidative stress of cells and the disorder of its own function.NOX family proteins are overexpressed in the pathological state and produce a large number of ROS,which are involved in the development and progression of a series of diseases such as atherosclerosis,hypertension,hypertrophy,tumor,and inflammation.Therefore,the study elucidated the pathogenic mechanism of NOX family,which is of great importance for the prevention,diagnosis and treatment of atherosclerotic plaques and related diseases.Aim Through the observation of vascular endothelial injury after nicotinamide adenine dinucleotide?NOX4?expression and effects of statins on the expression of NOX4,the stability of plaque in research of statins.With the mechanism of preventing coronary artery interventional therapy?PCI?restenosis,it will provide new research directions for improving plaque stability and preventing PCI restenosis at molecular level.Methods1.Research object.30 mice of 8 week old apoE gene defect(apoE^-/-)were selected and the body mass was250-300g.Then randomly divided into A/B/C three groups,10 of you,all mice were high fat diet?including 15%fat,0.25%cholesterol,84.75%base feed?.Group A:control group,group B:operation group,group C:intervention group.The mice were killed at the end of the 20 week.2.Research Indicators?1?histopathological changes of plaque were observed after HE staining.?2?immunohistochemical method was used to detect the expression of alpha-SMA and CD34 in atherosclerotic plaques.?3?RT-PCR method was used to detect the expression of NOX4mRNA in carotid artery tissue,and Western Blot was used to detect NOX4protein expression in carotid artery tissue.Results 1.pathology detection:HE staining in control group with small artery lumen plaque formation,operation group HE staining showed the carotid artery wall is not smooth,within the lumen of AS plaque,intimal surface is not smooth,the endothelial cells are not continuous,or lack of smooth muscle cell proliferation disorder.The plaque formation of carotid artery plaque in the intervention group was less than that of the B group,and the degree of disorder was more irregular than that of the B group.2.immunohistochemical staining:immunohistochemical staining showed that the expression of MOMA-2 and CD34 was localized in the plaques,and the operation group was significantly higher than that in the statin intervention group.There was a significant difference between the two groups?P<0.05?.The expression of NOX4 and protein in the3.operation group was further increased than that in the statin intervention group?P<0.05,P<0.05?.ConcluSion?1?The expression of NOX4 in the vascular endothelial cells was increased after the balloon injury of the carotid artery.?2?Atorvastatin inhibits neovascularization after arterial endothelial injury,and its mechanism may be related to the reduction of NOX4 expression.