| ObjectivesAcute Myocardial Infarction (AMI) is a serious type of coronary heart disease.In recent years, the incidence of AMI has been increasing quickly and becoming oneof the main reasons of Sudden Cardiac Death. With lots of serious complications thatcan be caused by AMI, the early intervention and treatment of patients is essential.AMI is mainly due to the formation of coronary artery occlusion, which makesSerious myocardial ischemia and hypoxia, leading to myocardial necrosis andapoptosis. As a cardiovascular protein, hspb7only shows its high expression in theheart, and plays a protective role in early myocardial cell damage. HSPB7wasrecently linked to heart failure, while whether HSPB7is involved in the AMI remainsunknown. Inflammatory response plays an important role in AMI which caused byvulnerable plaque rupture and thrombosis. In AMI, Pravastatin inhibits theinflammatory cell accumulation and endothelial cell adhesion to achieve itsanti-inflammatory effects.In order to provide a theoretical basis for the positive effects ofPravastatin when the acute myocardial infarction happens, this paper focus on theeffect of Pravastatin on the Expression of HSPB7in AMI. Methods1.120pcs healthy mature SD rats with the weight215-325g/pc and the age6-8weeks old respectively.The80AMI rats were randomly divided into acute myocardialinfarction group（AMI）, and Pravastatin group（P）, the40SD rats in sham operationgroup（SH）,then subdivide each group into group1h,3h,6h and12h.2.100g/L Chloral hydrate were injected into abdomen to anesthetize the ratswhich had been weighed. Under the condition of respirator, ligated the left coronaryartery to induce the acute myocardial infarction model of rats. SH was not ligated butthreaded; AMI was created by ligation of the1eft anterior descending coronary artery;Group P created by ligation of the1eft anterior descending coronary artery with aPravastatin of0.5mg/（kg·d），the other groups were given the same amount normalsaline via gavage. The myocardial tissue from left ventricular infarcted border zonewas harvested at each time interval，while the corresponding myocardial tissue insham-operated rats was harvested3.The expression of HSPB7protein and mRNA were detected byimmunohistochemistry and RT-PCR respectively.4.Analyse the data by exploiting SSPS17.0. All the quantitative data werepresented as means士standard error(x±s). Multiple comparisons were completedby using the one way analysis of variance (ANOVA) and the sattistical significanceof differences between the two groups was assessed with the least-significantdifference(LSD) test. Sattistical significance was set at α<0.05.Results1. The morphological changes of myocardial tissues The morphologicalchanges of myocardial tissues are as follows:group SH showed traces of brownparticles composing, mainly distributed in the cell periphery;group AMI showed alarge necrotic myocardial cells, and a moderate amount of brown particles, both in theperipheral and central area;slice group P witnessed a certain amount of visiblenecrotic cells and a large number of brown particles, mainly distributed in the centralcell.2. Compared with SH groups,the expressions of HSPB7mRNA and proteinwere higher in the AMI groups and P groups（P＜0.01）. All the above indexes exhibited an ascending tendency at1h after AMI，reached peak value at3h afterAMI，and remaining detectable up to12h after AMI. The P groups were still higherthan those in the AMI group.conclusions1. In the infarct and border zone,the expression of HSPB7protein and mRNAincreased significantly after acute myocardial infarction.2. Pravastatin can stimulate the expression of HSPB7protein and mRNA in theinfarct and border zone, resulting in improving the antioxidant capacity bymyocardial cells in the early AMI and building up cytoskeletal stability and resistanceon ischemia-reperfusion’s injury to the prevent apoptosis. |
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