| Background and objectivesWith the growing popularity of the thrombolytic treatment myocardialinfarction, percutaneous transluminal coronary angioplasty revascularization surgeryin clinical practice.Myocardial infarction mortality in patients with acutestage decreased significantly, But myocardial ischemia-reperfusion injury is a keyfactor in the effect of reperfusion therapy. Therefore, how to reduce the effects ofischemia and reperfusion injury myocardium become a new target for prevention andtreatment of ischemia-reperfusion injury. Currently the mechanism ofischemia-reperfusion injury has not been elucidated, studies have indicated thatischemia-reperfusion injury and free radical injury, calcium overload, leukocyte-induced inflammatory response, energy metabolism, apoptosis, microvasculardysfunction and so on. Free radical damage may be caused mainly due toischemia-reperfusion injury, radical oxidation has, easy and various cellularcomponents such as membrane phospholipids structure, proteins, nucleic acids andother oxidation reactions. Uncoupling protein (UCPS) is a proton transporter proteinson the inner mitochondrial membrane, while the increase in mitochondrial freeradicals can transport protons into the mitochondrial membrane, thereby reducing theoxidative damage of free radicals. Clinical studies have shown that angiotensinreceptor antagonist losartan can reduce myocardial infarct size, ventricular arrhythmias, improving myocardial remodeling and improve long-term prognosis ofpatients with myocardial infarction, between the role of these beneficial effects offree radical damage is associated with the decrease association is unclear. Therefore,this study reperfusion injury model of myocardial uncoupling protein2(UCP2)expression, given valsartan pretreatment, detection of myocardial uncoupling protein2(UCP2) expression and detection of superoxide dismutase (SOD) activity andmalondialdehyde (MDA) concentration, the effect of valsartan may reperfusion ofischemic myocardial protection mechanisms, experimental and theoretical studiesprovide evidence for the drug treatment. explore its possible mechanism ofmyocardial protection for drug therapy through the establishment of ischemiaexperimental evidence and theoretical research.Methods1Divide45weighing200-250g,6-8weeks old, healthy male adult SD ratswere randomly into three groups: sham group (SH group, n=15), ischemicreperfusion group (IR group, n=15), valsartan pretreatment group (X group, n=15).2After the rats were weighed, and10%chloral hydrate anesthetized rats byintraperitoneal injection of a solution, giving ventilator-assisted breathing, wearingthe sham group without ligation, ischemia-reperfusion group and valsartan groupwere pretreated coronary ligation left anterior descending artery after30min, andthen lift the ligation and reperfusion120min. Myocardial ischemia-reperfusion injurymodel. Valsartan pretreatment group received valsartan (30mg/kg),1times/day,orally for4weeks, and the remaining two were given an equal volume of saline.3After myocardial ischemia-reperfusion injury model is successfully established,test the concentration of SOD and MDA.4After HE staining, using an optical microscope, observing morphologicalchanges of myocardial cells.5in each group of myocardial ischemia-reperfusion group and valsartanpretreatment taken from the left ventricle myocardium ischemia and reperfusion inthe sham group to take appropriate ventricular region, Western blot, RT-PCR assayin UCP2protein and mRNA expression. 6Statistical analysis was performed using SPSS17.0.3groups ofmalondialdehyde content, SOD activity, UCP2protein and mRNA expression werecompared using ANOVA, pairwise comparisons using LSD-t test. Each test level α=0.05.Results1myocardial tissue morphological changes: SH group was visible neatbundles of muscle fibers, no inflammatory cell infiltration, no necrosis; IR groupshowed congestion, congestion, swelling of the muscle fibers, myocyte disarray, redblood cells and inflammatory cell infiltration, visible myocardial interstitial edemaand focal necrosis; X mild swelling of myocardial fibers, compared with the modelgroup myocardial cells arranged in neat, small amounts of myocardial interstitialvisible red blood cells and inflammatory cell infiltration, interstitial edema and mildnecrosis to a lesser extent.2malondialdehyde content, ischemia-reperfusion group, valsartan pretreatmentgroup were higher than the sham group (P <0.01), valsartan pretreatment group thanin ischemia-reperfusion group (P <0.01) The differences were statistically significant.SOD activity, ischemia-reperfusion group, valsartan pretreatment group werereduced (P <0.01) than the sham group, valsartan group than pretreatmentischemia-reperfusion group (P <0.01), the differences were statistical significance.The relative expression of UCP2mRNA, and ischemia-reperfusion group, valsartanpretreatment group were higher than the sham group (P <0.01), valsartan pretreatmentgroup than in ischemia-reperfusion group (P <0.01)). Expression of UCP2protein,ischemia-reperfusion group, valsartan pretreatment group were higher than the shamgroup (P <0.01), valsartan pretreatment group than ischemia-reperfusion group (P<0.01).conclusionsvalsartan can increasing the expression of UCP2, reducing the express ofoxygen free radicals, which play a role in the protection of myocardialischemia-reperfusion injury. |
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