| Background:Cardiac ischemia-reperfusion injury(coronary recanalization or heart transplantation)can cause myocardial tissue necrosis,and the response of inflammatory that caused by necrosis can affect the function of normal cardiac cells,and can even lead to heart failure.Scientific researches have shown that PARP-1(poly ADP-ribose polymerase)can regulate the process of cells necrosis and apoptosis when they are stimulated by physical and chemical factors,and through this way to adjust their function.In this experiment,the allotransplantation of SD rats was used as a myocardial ischemia-reperfusion model.The level of PARP-1 and cardiac injury markers,apoptotic markers were measured after cardiac transplantation to explore the beneficial effects of Poly(ADP-ribose)polymerase inhibition against the reperfusion injury in heart transplantation,and provide new theoretical basis and ideas to guide treatment for the patientes thoes who are suffering from acute myocardial infarction and heart transplantation.Methods:Male SD rats weighing 260-320g were randomly divided into donor group and recipient group.The donor components contains two groups those are PJ34 group and NaCl group;and the recipient components were divided into transplantation group and blank group.Rats in the PJ34 group were injected intraperitoneally with PJ34(PJ34-hydrochloride).The NaCl group was given an intraperitoneal injection of normal saline.The rats in the recipient group were treated accordingly and the control group was not treated.The cervical heterotopic cannula is used to build the heart transplantation model,after the translated hearts are suffering from ischemia and reperfusion,the plasma and transplanted hearts were collected for testing.Involved techniques such as immunofluorescence staining,western bloting and enzyme-linked immunosorbent assays ect.Results:The expression levels of lactate dehydrogenase(LDH),creatine kinase(CK),cardiac troponin T(cTnT)and cardiac troponin I(cTnI)in serum were significantly higher in the NaCl group than the PJ34 group;And the PJ34 group was slightly higher than the control group,with statistical significance between the groups.Tetrahydroxydecenoic acid(4-HNE)and malondialdehyde(MDA)are lipid peroxides in the Serum,the most significant increase in the expression level is the NaCl group.The application of PARP-1 inhibitors(PJ34)can effectively reduce the increase of lipid peroxides.The enrichment factor(EF)in the myocardial tissue was significantly higher in the PJ34-treated group,and its increase range was 5-6 times that of the NaCl group and the Control group,while the Nacl group Compared with the Control group,the increase range of EF was only 1.23 times.Those indicated that the application of PJ34 had an effect on the EF content after myocardial ischemia and reperfusion in rats.The PARP-1 inhibitor(PJ34)significantly inhibited the expression of PARP-1 in the heart after ischemia-reperfusion.The expression of PARP-1 was significantly lower than that in the control group and the NaCl group.The Western blotting results were consistent with the results of immunofluorescence.Using PARP-1 inhibitor(PJ34)can promote the expression of Caspase3 and Caspase8 which are apoptosis proteins in myocardial.The expression levels of Caspase3 and Caspase8 were significantly increased from the Control group,the NaCl group to the PJ34-treated group.Gray-scale analysis confirmed this trend,and the results are same as immunofluorescence.Conclusion:In the heart ischemia-reperfusion model(heart transplantation model)of rats,the use of PARP-1 inhibitor(PJ34)can effectively reduce the expression of myocardial injury markers such as myocardial enzymes and serum enzymes,and reduce the lipid peroxidation of cells.At the same time,the PARP-1 inhibitor(PJ34)can change necrosis into apoptosis in some ways.The PARP-1 inhibitor has myocardial protection to against the reperfusion injury in heart transplantation. |
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