大鼠心肌缺血再灌注中IL-10、MPO的变化及关系

目的　探讨大鼠心肌缺血及再灌注过程中血清白介素 10 (IL 10 )、心肌组织中髓过氧化物酶 (MPO)活性的变化和相互关系。方法　将大鼠随机分成假手术组、缺血 /再灌注组 (对照组 )、甲基强的松龙组 (药物组 )三组。在心肌缺血前用甲基强的松 (30mg/kg)对治疗组大鼠预处理。分别测定缺血 0 .5h、再灌注 0 .5h及 2h血清中IL 10浓度、心肌组织MPO活性。结果　IL 10自缺血 0 .5h、再灌注 0 .5h至 2h呈逐渐升高趋势 ,再灌注 2h与再灌注前相比较具统计学差异 (P <0 .0 5 ) ,对照组较假手术组、药物组较对照组各时段IL 10明显升高 ,再灌注后具有统计学差异 (P <0 .0 5 )。MPO在对照组中自缺血 0 .5h、再灌注 0 .5h至 2h呈逐渐升高趋势 ,其中再灌注 0 .5h与再灌注前相比具有统计学差异 (P <0 .0 1) ;对照组与假手术组比较各时段MPO明显升高 ,具有统计学差异 (P <0 .0 5 ) ;药物组与假手术组相比各时段均升高但无统计学差异 ;药物组MPO各时段比对照组明显降低 ,具有统计学差异 (P <0 .0 5 )。IL 10与MPO存在显著性负相关 (r =0 .0 6 4 9,P <0 .0 1)。结论　在大鼠心肌缺血再灌注中 ,甲基强的松龙可促进内源性IL 10大量释放 ;IL 10可抑制MPO的活性 ,减少炎性反应 ,发挥心肌保护作用

Changes of Interleukin-10 and MPO,CK-MB During Myocardial Ischemia and Reperfusion in Rats

Objective To investigate the changes of interleukin 10(IL 10)and MPO and their relation in acute myocardial ischemia and reperfusion.Methods Sixty three rats were divided randomly into three groups,including 21 sample rats and 21 control rats who received i.v.bolus placebo,and 21 administration rats who received i.v.blous methylprednisolone before ischemia.The control and administration groups were subjected to myocardial ischemia ischemia and reperfusion.Plasma IL 10 was measured with ELISA at 0.5 hour after ischemia and 0.5 and 2 hours after reperfusion,meantime myocardial MPO were measured at respective time points.Results Serum concentration of IL 10 increased gradually after 0.5 hour of ischemia,and was significantly increased at 2 hours after reperfusion in both control and control and administration groups at 2 hours after myocardial reperfusion( P <0.01).Administration of methylprednisolone significantly increased IL 10 levels compared with that in control group at 0.5 to 2 hours after reperfusion.In the administration rats,the levels of MPO were significantly lower than those of control group( P <0.05).In addition,the expression of IL 10 negatively correlated with PRO( P <0.01).Conclusion The present findings indicated that IL 10 serves to protect the ischemia and reperfused myocardium by reducing production of MPO and mythylprednisolone enhance highly release of endogenous IL 10.