| Backgrounds and aimsAcute myocardial infarction (AMI) is a serious disease threat to human life and health. As medical technology advances, the survival rate of acute myocardial infarction was significantly increased. Atherosclerosis is the occurrence of acute coronary events based on the pathological.Recent studies show that plaque rupture, plateletaggregation, thrombosis is the acute coronary syndrome (ACS). ACS is the place where plaque rupture is the most important initial factor, With further research and found that the inflammatory response of atherosclerosis (AS) of the core elements. First of all acute myocardial ischemic event caused by myocardial ischemia-reperfusion injury, Its mechanism is currently considered the main and leukocyte activation, oxygen free radicals and calcium overload. The most important mechanism is the activation of white blood cells, Especially the white blood cell-mediated microvascular injury play an important role in ischemia-reperfusion injury, Animal experiments have found no-reflow phenomenon is the basis of the pathophysiology of neutrophil activation and proinflammatory cytokine release. This shows that inflammatory response in acute myocardial ischemic events. Inflammatory response involves the activation of endothelial structure and function stability, cell adhesion factor, the interaction between inflammatory mediators. Statin drugs appear to the treatment of cardiovascular diseases brought "epoch-making revolution." Large-scale multicenter randomized controlled trial from the perspective of evidence-based medicine statins confirmed the clinical value. In recent years a large number of studies have shown that statins have many beneficial effects beyond lipid lowering, particularly in the anti-inflammatory effect. This study is to produce myocardial infarction rat model, with Fluvastatin intervention, measure Myocardial infarction nuclear transcription factors (NF-KB) and soluble cell adhesion molecule (sICAM-1) expression and correlation between them, Compared with the control group, To study the mechanism of Fluvastatin by inhibiting the inflammatory response after myocardial infarction in rats.Materials and methods1.60 male Wistar rats in (240±20g)body weight with a clean and healthy were randomly divided into 2 groups:normal group (n=10) and surgical group (n=50). Myocardial infarction produced by ligating the left anterior descending artery (LAD), sham operation group only wear line but not tied. Surgical group were divided into sham group, myocardial infarction group and Fluvastatin treatment group. After 24 hours survival of 38 rats, were randomly divided into two groups:myocardial infarction group (n=20) and Fluvastatin treatment group (n=18). Fluvastatin intervention group were given atorvastatin fluoride 20mg/(kg.d) of sterile distilled water, sham operation group and the myocardial infarction group was the same amount of normal saline.2.After 4 weeks of each group were sacrificed remove the myocardium of rats. Normal (N) and sham 2group (J) no difference between sites, The myocardial infarction group (M) and Fluvastatin group (F) were replaced with 1 or 4 marginal zone of myocardial infarction,2 or 5 on behalf of myocardial infarction, myocardial infarction 3or 6 on behalf of the remote area, Three myocardial tissues were taken from preserved in liquid nitrogen into the-80℃.3.Cardiac tissue were used for immunohistochemical analysis and reverse transcription-polymerase chain reaction (RT-PCR) semi-quantitative analysis.Reslults1.General:After 4 weeks, the survival of the rats, the normal group 10, sham group 9, myocardial infarction 8, fluvastatin group 11. Sham form of rat heart full of dark red eye view;AMI the naked eye view of rat heart ventricular infarct was thinning, subsidence, milky white.2.1mmunohistochemical Analysis:The group of non-infarcted myocardial NF-κB p65 and sICAM-1 expression changes before and after intervention:Normal group did not express NF-κB p65, sICAM-1 expressed little or no expression, Both myocardial infarction group significantly increased. Fluvastatin group had significantly lower expression of the two groups.3.RT-PCR analysis:Image analysis and statistical treatment showed that:NF-κB p65 and sICAM-1mRNA in the normal group and sham group showed low expression and no significant difference between them (P>0.05). Both in myocardial infarction group was significantly increased (P<0.01). Compared with the myocardial infarction control group, both fluvastatin group was significantly reduced.Conclusions1.Fluvastatin can reduce non-myocardial infarction expression of inflammatory molecules, thereby improve the non-infarcted area of the inflammatory response.2. Fluvastatin non-infarcted myocardium can reduce expression of NF-KBp65 and sICAM-1mRNA the concentration levels, Fluvastatin may reduce inflammatory response around the non-infarct zone. The anti-inflammatory mechanism may be down the two concentrations. |
PDF Full Text Request