LAUSR

Purpose: To investigate the effect of morphine preconditioning on myocardial ischemia reperfusion injury in heart failure rats, and the mechanism(s) of action involved Methods: Seventy-two healthy male Sprague-Dawley rats were assigned to 4 groups: sham, model, morphine-preconditioning and SB203580 inhibitor groups, each with 18 rats. The expressions of P-p38, p-glycogen synthetase kinase-3, and p-gap junction protein 43 in rat myocardial cells were assayed by Western blotting. The mRNA expression levels of Bcl-2 and Bax, and Bcl-2/Bax were determined using real-time fluorescence quantitative PCR. Results: The expression levels of P-p38, p-glycogen synthetase kinase-3, p-gap junction protein 43, Bcl-2 mRNA and Bcl-2/Bax were significantly higher in the pretreatment group than in the model group, while Bax mRNA was significantly lower (p < 0.05). Moreover, the mRNA expression levels of P-p38, pglycogen synthetase kinase-3, p-gap junction protein, Bcl-2, and Bcl-2/Bax in inhibitor-treated rats decreased significantly, when compared to the values for pretreatment rats; furthermore, Bax mRNA was markedly upregulated (p < 0.05). Conclusion: Morphine preconditioning significantly inhibits the expressions of GSK-3β and Cx43 signaling proteins, as well as apoptosis-related gene, Bcl-2 and Bax. In addition, it inhibits the apoptosis of rat cardiomyocytes, and reduces myocardial injury, after ischemia reperfusion, via activation of the p38 MARK signaling pathway. This provides a new strategy for clinical reduction of myocardial injury after ischemia-reperfusion.