Effect of propofol on myocardial injury induced by hepatic ischemia/reperfusion in rats and the role of PI3K/Akt signaling pathway

Objective To investigate the effect of propofol on myocardial injury induced by hepatic ischemia/reperfusion （I/R） in rats and the role of PI3K/Akt signaling pathway. Methods One hundred and two male SD rats weighing 250-280 g were randomly divided into 5 groups： Ⅰ sham operation group （group S, n =6）, ⅡI/R group （ n = 30）, Ⅲ propofol group （group P, n = 30）, Ⅳ propofol ＋ LY294002 group （group P＋ LY, n =18）, and Ⅴ propofol ＋ dimethylsulfoxide group （group P＋ DMSO, n = 18）. Hepatic I/R was produced by occlusion of hepatic pedicle for 30 min followed by reperfusion in group Ⅱ - Ⅴ. Propofol 12 mg/kg, propofol 12mg/kg ＋ LY294002 （a specific PI3K inhibitor） 1.5 mg/kg, and propofol 12 mg/kg ＋ DMSO 0.5 ml were injected I.v.via femoral vein at 10 min before ischemia in group Ⅲ -Ⅴ respectively, and then propofol was infused I.v. At a rate of 30 mg· kg- 1 · h - 1 and the administration was stopped before the rats were sacrificed in group Ⅲ - Ⅴ . At 0,30, 60, 120, and 240 min of reperfusion （T1-5） in group Ⅱ and Ⅲ , and at T3.5 in group Ⅳ and Ⅴ , six rata were sacrificed and myocardial tissues were taken for determination of the total Akt （t-Akt） and phosphorylated Akt （p-Akt） expression and Bcl-2 expression and apoptosis were detected at T3. The hepatic tissues were taken for microscopic examination. The rats were sacrificed at T1 and the parameters mentioned above were detected in group Ⅰ . Results Compared with group Ⅰ , p-Akt expression and apoptosis rate were significantly increased in the other4 groups, and Bcl-2 expression was up-regulated in group Ⅱ , Ⅲ and Ⅴ （P 〈 0.05）. Compared with group Ⅱ , p-Akt and Bcl-2 expression was up-regulated, and the apoptosis rate was significantly decreased in group Ⅲand Ⅴ （ P 〈 0.05）. Compared with group Ⅲ , p-Akt and Bcl-2 expression was down-regulated, and the apoptosis rate was significantly increased in group Ⅳ （ P 〈 0.05）. The microscopic examination showed that the injury to the hepatic tissues was less severer in group Ⅲ and Ⅴ than in group Ⅱ and Ⅳ. Conclusion Propofol can attenuate myocardial injury induced by hepatic I/R in rats by activation of PI3K/Akt signaling pathway. Key words: Propofol;  1-Phosphatidylinositol 3-kinase;  Protein-serine-threonine kinases;  Liver; Reperfusion injury;  Myocardium