Effect of dexmedetomidine on PI3K/Akt/GSK-3β signaling pathway during apoptosis in cardiomyocytes of rats with severe scald

Objective To evaluate the effect of dexmedetomidine on phosphatidylinositol 3-kinase(PI3K)/protein kinase B(Akt)/glycogen synthase kinase-3 beta(GSK-3β)signaling pathway during apoptosis in cardiomyocytes of rats with severe scald. Methods Twenty-four healthy adult male Sprague-Dawley rats, weighing 220-280 g, were divided into 3 groups(n=8 each)using a random number table method: control group(group C), severe scald group(group S)and dexmedetomidine group(group D). Thirty percent of the total body surface area was shaved on the back and then exposed to 94 ℃ water(with 37 ℃ warm water in group C)for 12 s to establish the model of third degree scald in pentobarbital sodium-anesthetized rats.Dexmedetomidine 30 μg/kg(2 μg/ml)was intraperitoneally injected immediately after scald in group D. Rats received anti-shock treatment by intraperitoneal injection of isotonic saline according to Parkland formula, and group C received no injection.Rats were anesthetized using the method previously mentioned at 12 h after treatment, and myocardial specimens of the left ventricle were rapidly excised and stored at -80 ℃ for determination of cell apoptosis(by TUNEL)and expression of P13K, phosphorylated Akt(p-Akt)and phosphorylated GSK-3β(p-GSK-3β)(by Western blot). Apoptosis index(AI)was calculated. Results Compared with group C, AI was significantly increased, and the expression of P13K, p-Akt and p-GSK-3β was up-regulated in S and D groups(P<0.05). Compared with group S, AI was significantly decreased, and the expression of P13K, p-Akt and p-GSK-3β was up-regulated in group D(P<0.05). Conclusion Dexmedetomidine inhibits apoptosis in cardiomyocytes through activating PI3K/Akt/GSK-3β signaling pathway in the rats with severe scald. Key words: Dexmedetomidine; MAP kinase signaling system; Apoptosis; Myocardium; Burns