| Objective: To investigate the effect of leptin on the regulation of apoptosis and the protective effect on rat myocardial ischemia reperfusion injury by signaling pathway at the level of tissue and molecular protein. Methods: 50 healthy male SD rats were randomly divided into five groups: A, B, C, D, E(10rats in each group). Group A was ischemia/reperfusion model group; group B was sham operation group which just opened the chest and without a vascular ligation; group C, D, E respectively was in low, median, high dose leptin group(the dose were 20μg /kg, 50μg/kg, 100μg/kg). Using Suture-occluded method to make the model of myocardial ischemia reperfusion injury rats, after 30 minutes for ischemia and after 24 hours for reperfusion to observe the pathologic changes of myocardial tissue of HE staining, Western Blot was used to observe leptin on PI3 K, AKT, NFκB, mTOR, Bcl-2 and Bax proteins, ELISA test the mitochondrial permeability transition pore(mPTP) in serum. Result: Compared with group B, myocardial histopathology of group A, C, D and E was characterized by obvious myocardial fibers disorder, inflammation cells infiltration, erythrocyte effusion. The expression of PI3 K, AKT, NFκB, mTOR and Bcl-2 were statistically significant(P < 0.05), but expression of mPTP and Bax were decreased significantly(P < 0.05); Compared with group A, HE staining pathological changes were significantly improved in group C, D, E. The expression of PI3 K, AKT, mTOR, NFκB, Bcl-2 and Bax were all in different degrees of increase, and the difference was statistically significant(P<0.05).Conclusion: Leptin pretreatment have a protection effect on myocardial ischemia reperfusion in rats, the protective mechanism may be related to the leptin cause the upregulation of the expression of mycardial’s PI3 K, Akt, mTOR,Bcl-2, NF κ B, and downregulation of mPTP, Bax expression. Promote myocardial cell survival, inhibition of apoptosis and decrease in mitochondrial permeability transition pore opening related. |
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