The effect of hyperbaric oxygenation on apoptosis in rats after middle cerebral artery occlusion / 中华物理医学与康复杂志

ABSTRACT

Objective To observe the effect of hyperbaric oxygenation (HBO) on apoptosis-inducing factor (AIF) and Caspase-3 levels in rats with permanent middle cerebral artery occlusion (MCAO),and to elucidate the apoptosis pathways.Methods Sixty Sprague-Dawley rats were subjected to permanent MCAO and then randomly divided into a control group and an HBO group,each of 30.Three hours later the rats of the HBO group were put into a hyperbaric cabin held at a pressure of 0.2 MPa for 9 hours.They inhaled supplementary oxygen at the 1st,3rd,5th,7th and 9th hour while the rats in the control group inhaled air at normal pressure.The neurological outcome was measured at the 3rd,13th and 72nd hour after the MCAO using Garcia scores.Apoptosis in the tissue of the ischemic penumbra,nuclear and mitochondrial AIF and Caspase-3 levels were measured at the 13th and 72nd hours after the modeling.Results The scores were significantly higher at the 13th hour than after the 3rd hour in both groups,and then even higher at the 72nd hour.Apoptosis was evident in the ischemic penumbra at the 13th and 72nd hours in both groups,but the number of cells was less at the 72nd hour than at the 13th hour in the control group.There was significantly less apoptosis in the HBO group than in the control group at the 13th hour.The average AIF level had significantly decreased in the nuclei and increased in the mitochondria by the 72nd hour compared with the 13th hour in both groups.The average levels of nuclear AIF at the 13th hour and the 72nd hour were lower than those in the mitochondria.But they were significantly higher in the HBO group than in the control group at the same time points.The levels of Caspase-3,normally zero,had increased by the 13th hour in both groups.The average level of Caspase-3 was significantly lower in both groups at the 72nd hour than at the 13th hour.Conclusions HBO can improve neurological function,inhibit the transfer of AIF from the mitochondria to the nucleus and reduce Caspase-3 levels.The mechanism may involve reducing apoptosis through caspase-dependent and caspase-independent pathways in the mitochondria.