Effects Of Emodin On Ischemia-reperfusion Injury Pig Myocardial Protection And Mechanism Of Inflammatory Response

Object:Myocardial ischemia-reperfusion injury is a complex multi-factor involved in the pathological process involves a number of links.Oxygen free radicals and the generation of inflammatory factors and myocardial ischemia-reperfusion injury.Inflammatory response(including leukocyte infiltration,inflammatory cytokines and the release of inflammatory mediators) in myocardial ischemia-reperfusion injury plays an important role.This study was designed to investigate the effect of emodin on myocardial ischemia-reperfusion injury and protective effect against the possible mechanism of inflammatory response.Methods:Choice of 12 Chinese miniature pigs were divided into three groups,namely control group,CVD group(carvedilol),emodin group.Balloon method used to plug animal model of ischemia-reperfusion.TTC staining of the scope of the changes in myocardial infarction and left ventricular ejection fraction(EF) changes.Detection of I / R before,I/R2h and I/R6h serum CK-MB and cTnI changes.Detection of I / R before,I/R2h and I/R6h serum, IL-6 and IFN-r changes.Western blot assay I/R6h complement C3, TNF-αand expression of myocardial HSP60.TUNEL staining of cardiomyocyte apoptosis.Immunohistochemical staining of myocardial MCP-1 expression.Result:This study confirmed that emodin can significantly reduce the I / R myocardial infarction after the scope of the protection and improvement of myocardial function,similar to its role and CVD, compared with the control group,the difference was significant(P <0.05).Emodin significantly inhibited I / R when the complement C3 activation and consumption,,IFN-r level,the degree of similarity with CVD,compared with reducing TNF-αthe control group were significantly different(P<0.05).Emodin also inhibited MCP-1 and HSP-60 expression,compared with the control group were significantly different(P <0.05).With CVD compared to the role of similarity between the two,no statistical difference.Conclusion:The above results show that emodin significantly inhibited I / R when the complement activation,the release of inflammatory mediators and the inflammatory response induced myocardial cell injury,inhibition of cardiomyocyte apoptosis, thereby protecting myocardial structure and function of cells, similar to its role and CVD.