Objective    To investigate the role and mechanisms of the PI3K/Akt signal pathway in the apoptosis of rat cardiomyocytes after ischemia and hypoxia due to severe burn injury.     Methods    Burn models of full-thick 30%TBSA burn injury were established by scalding rat back in hot water. The activation of the PI3K/Akt signal pathway was observed by Western blotting

and myocardial apoptosis was assessed by TUNEL. Cultured rat cardiomyocytes under ischemic/hypoxic conditions were divided into the control group

the ischemia and hypoxia group

and the LY294002 or IGF-1 treatment group. The apoptosis of cardiomyocytes were assessed by ELISA. The caspase-3 activity was measured by DEVD fluorescence. The transcriptional activity of p53

Bax was assessed by RT-PCR.     Results    After severe burn

PI3K and pAkt expressions increased gradually in the rat myocardial tissue

and reached a peak at 3 h postburn. At 3 h postburn

the apoptosis increased significantly in rats. When the PI3K/Akt pathway was specifically inhibited by LY294002

the myocardial apoptosis increased significantly in the burn group as compared with the control group (P0.05). Cultured cardiomyocytes after ischemia and hypoxia showed the following changes：  increased apoptosis

gradually enhanced caspase-3 activity

gradually increased p53 and Bax mRNA expressions. Compared with the ischemia and hypoxia group

blockade of the PI3K/Akt pathway with LY294002 increased the number of apoptotic cardiomyo-cytes

caspase-3 activity

and p53 and Bax mRNA expression significantly (P0.05). After activation of the PI3K/Akt pathway with IGF-1

caspase-3 activity decreased significantly (P0.05)

as compared with the ischemia and hypoxia group.     Conclusion    The PI3K/Akt signal pathway plays anti-apoptotic role in ischemic/hypoxic cardiomyocytes. PI3K/Akt pathway regulating p53 and Bax expression is probably the mechanism of anti-apoptosis

which can suppress the activity of caspase-3 and decrease the number of apoptotic cardiomyocytes.