Effects Of Endogenous Interleukin-10 During Myocardial Ischemia And Reperfusion In Rats

Background and objective: ischemia and reperfusion injury (IRI) is an important problem that must be soluted in clinic. The mechanism about IRI isn't be illustrated assuredly exception for production of oxygen free radicel, calcium overload and neutrophil infiltration. The recently studies denomstrated that the cytoleukins released heavily during myocardial ischemae and reperfusion. Among them, interleukin-10(IL-10) producted from various cell and possessing various function is anti-inflammatory and immunosuppressor cytokine ,playing an key role in myocardial ischemia and reperfusion. We investigated the change and role of endogenously produced IL-10 in acute myocardial ischemia and reperfusion and methylprednisolone influencing on production of endogenously IL-10 in our experimentMethods: we put equally 63 rats into three groups at random, including 21 sham rats, 21 control rats who received i.v. bolus placebo and 21 administration rats who received i.v. bolus methylprednisolone before ischemia, among them control and administration groups subjected to myocardial ischemia and reperfusion. Plasma IL-10 by ELISA was measuredat 0.5 hour after ischaemia and 0.5, 2 hours after reperfusion, meantime plasma CK-MB(creatine phosphokinase-KB) were measured with the use of commercial kits and myocardia infarct size were analysis, while myeloperoxidase (MP<0). serum Nitric oxide synthase and inducible Nitric oxide synthase (Nos, iNos)were measured at respective time P<0ints.Result: IL-10 change little in sham group. Significant levels of IL-10 were produced in both control and administration groups from ischemia 0.5 hour to 0.5 hour, 2 hours after myocardial reperfusion (control group: F=26.075, P<0.01; administration group: F=39.263, P<0.01), while Serum concentration of CK-MB increased gradually and significantly from ischemia 0.5 hour to 0.5 hour, 2 hours after myocardial reperfusion(ischemia 0.5h group: F=85.383, P<0.05; reperfusion 0.5h group: F=64.923, P<0.01; reperfusion 2h group: F=131.727, P<0.01). Notably, administration of methylprednisolone increased IL-10 levels which were significantly higher than that in control group at 0.5 ischemia to 0.5 and 2 hours after reperfusion. In the administration rats, the increase of CK-MB were delayed and the levels were significantly lower than those of control group (p<0.05) . Meantime concentrations of serum Nos, iNos significiantly rose following prolonging reperfusion time(Nos: control group F=25.011, P<0.05; administration group F=3.526, P<0.05; iNos: control group F = 8.340, P<0.05, administration group F=13.601, P<0.01). myocardial MP<0 signifciantly rose following prolonging reperfusion time(MP<0: control group F=4.153, P<0.05; administration groupF=8.725, P<0.01), but declined slightly whlie more reperfusion extending. Increase of IL-10 attenuated neutrophil infiltration into the reperfusion tissues after reperfued and reduced infarct size and myocardial necrosis. In addition, the expression of IL-10 correlated with CK-MB, MP<0, Nos, iNos (P<0.05) except that the expression of IL-10 correlated with myocardial infarct size (p>0.05) .Conclusion: The present findings indicated that endogenous IL-10 serve to protect the ischemia and reperfued myocardia and mythylprednisolone enhance highly release of endogenous IL-10. IL-10 is an imP<0rtant factor of inhibiting inflammatory resP<0nse associated with myocardial reperfusion infarction.