Effect of dexmedetomidine on PI3K/Akt/GSK-3β signaling pathway during apoptosis in cardiomyocytes of rats with severe scald / 中华麻醉学杂志

ABSTRACT

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 SpragueDawley 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.