A Comparative Study On The Mechanisms Of Inhibiting Ischemia-reperfusion Myocardium Injurythrough IGF-1Postconditioningand Ischemic Postconditioning

Objective1.Compararing IGF-1postconditioning with ischemia-reperfusion tomake sure whether IGF-1have protective effects on ischemia-reperfusionmyocardium.2.Compararing with ischemia postconditioning,to make sure theprotective effect and extent of IGF-1postconditioning onischemia-reperfusion myocardium.3.To explore their possible inhibiting-mechanisms on myocardiumapoptosis by compararing IGF-1postconditioning with ischemiapostconditioningMethods48SD rats were randomly and evenly divided into4groups (12each):sham-operation group (sham), ischemic/reperfusion group (I/R), ischemicpostconditioning group (I-POST), and IGF-1postconditioning group(IGF-1-POST). The models were established by repeatedly ligating. Exceptthe sham group, rats in the other three groups kept ischemic for45min and then they were continuously reperfused for120min. During the first30minof the reperfusion period, the cardiological electrical activity was recorded.At point of120th min, the hemodynamic parameters were monitored; Thedegree of myocardial damage in pathology was observed by HE staining;The apoptosis was detected by TUNEL; The TNF-α, IL-6, and IL-10level inthe serum were detected by ELISA;Pser-133-CREB and the expression ofBcl-2protein was monitored by Western blotting and immunohistochemicalmethods.ResultsCompared with that of I/R group, the hemodynamic parameters (HR、SBP、DBP、LVSP、LVEDP、±LVdp/dtmax) of rats in I-POST group andIGF-1-POST group was improved; The ventricular premature beats and theduration of ventricular arrhythmia decreased;The degree of myocardialdamage in pathology lessened and the number of apoptosis reduced;TNF-αand IL-6level in the serum got lower while IL-10level became higher；Theexpression of Pser-133-CREB and Bcl-2protein increased significantly(P<0.05).2.Compararing IGF-1postconditioning with ischemia postconditioning,ischemia postconditioning can decrease the ventricular premature beats andthe duration of ventricular arrhythmia further; and IGF-1postconditioningcan decrease inflammation further.However, at other aspects mentionedabove there were no statistical differences between the two groups (P>0.05). Conclusion1.Myocardial ischemia reperfusion may increase myocardial injuries,and IGF-1has postconditioning protective effects on ischemia-reperfusionmyocardium.2.The extent of IGF-1postconditioning protective effects might besimilar to that of ischemic postconditioning.3.The anti-apoptosis effects of IGF-1postconditioning and ischemicpostconditioning might be related with the high level expression of Pser-133-CREB and Bcl-2protein.