Study Of TRAIL And Fas L During Ischemia-reperfusion Injury Effect On Myocardial Tissue Induced By Acute Myocardial Infarction

MI is a kind of diseases which we know as ischemic necrosis of myocardial tissue. Onthe basis of coronary artery disease, the blood of coronary artery drastically reduce orinterrupt, then serious and persistent acute ischemia of myocardium occur which lead toischemic necrosis of myocardial tissue. After coronary artery atherosclerotic plaque ablationor cutthrough of vessel, blood intrusion into the heart again, which induce myocardialischemic reperfusion injury, and the injury may lead to myocardial cell necrosis.The damage of ischemic reperfusion is serious. In the cell nucleus of necrotic tissue,DNA chain is destroyed, PARP-1was activated largely, PAR polymer accumulated in thenucleus and cytoplasm. The change of above lead to convert of mitochondrial membranepotential and membrane permeability and release of cytochrome C and other apoptosis relatedproteins into the cytosol from mitochondria. Then the caspase cascade effect was activated,meanwhile TRAIL and Fas L etc. necrosis factor activated at large.Objectives:This study aimed to investigate if the two necrosis factors, TRAIL and Fas L, can beconsidered as blood indicators for the ischemia-reperfusion damage after acute myocardialinfarction. And provide a reference for the two factors in defining the myocardial injury inclinic. Simultaneously we provide a preliminary study on the cell death mechanism includingPARP1and TRAIL with Fas L.Methods:The bloods from rat both in acute myocardial infarction groups and sham operationgroups were collected. Then PCR and Western blot were carried out to detect the levels ofTRAIL and Fas L, two kinds of necrosis factors, in rats, serum. At the same time, detectingthe changes of TRAIL and Fas L in bloods of myocardial infarction of reperfusion injury afterinfarction, we will analysis changes of the above two factors. In addition, we cultured HCMcells in vitro. At fast, the cells were cultured in serum-free medium and were treated bydifferent concentrations of hydrogen peroxide for1hour. Secondly, hydrogen peroxide was removed and the cells were cultured in serum-supplemented medium for6hours. Then theHCM cells were collected. At last PCR and Western blot were carried out to detect thechanges of TRAIL and Fas L level.Result:The detection of collected blood samples of treatment groups and controls showing thatthe level of active TRAIL in myocardial infarction is significantly lower than that in controls,but Fas L is on the contrary. In vitro, the results of the induction HCM cells showed, Fas Lexpression presented upward trend following the accumulation of reactive oxygen species, butTRAIL not.Conclusion:The activation of TRAIL is negative correlation with myocardial infarction andreperfusion injury, but Fas L is positively correlated. The above view have also beenconfirmed by experiment in vitro in which we deal HCM cells with hydrogen peroxide. PARP1, TRAIL and Fas L were involved in the mechanism of myocardial reperfusion of acutemyocardial infarction.