Study On Peroxisome Proliferator-activated Receptor-? Involved In Myocardial Protection Mechanism Of Sevoflurane Postconditioning

Objective: To observe the effect of sevoflurane on PPAR-? in reperfusion myocardium and study the role of PPAR-? in sevoflurane postconditioning against myocardial ischemiareperfusion injury.Methods: Male C57BL/6 mice were randomly allocated into four groups(n=5 each): Control group,Sevoflurane postconditioning(SPostC)group,Sevoflurane postconditioning+PPAR-? inhibitor(SPostC+GW9662)group,PPAR-? inhibitor(GW9662)group.All the groups establish the model of mice myocardial ischemia-reperfusion injury(30 min of ischemia and 120 min of reperfusion)in vivo,mice with myocardial ischemia received 3.4% sevoflurane for 15 min at the onset of reperfusion as the sevoflurane postconditioning,and all the groups inject inhibitor or placebo intraperitoneally at 30 min before ischemia.The heart rate(HR)and mean arterial pressure(MAP)of mice were measured before ischmia and after reperfusion.After experimental time out,heart of mice was excised,myocardial infarct size and PPAR-? transcriptional activity were tested in the early(30min)and late(120min)reperfusion.Results: Compared with Control group,myocardial infarct size reduced(P<0.05)significantly and PPAR-? transcriptional activity increased(P<0.05)in SPostC group,PPAR-? transcriptional activity in 120 min reperfusion is higher than 30 min.myocardial infarct size and PPAR-? transcriptional activity had a little change(P>0.05)in SPostC+GW9662 group and GW9662 group compared to control group.HR and MAP also have no difference between the groups of each point.Conclusion: Sevoflurane postconditioning can reduce myocardial infarct size via activating PPAR-? and improving its transcriptional activity during myocardial ischemia-reperfusion injury.