Mechanism and effect of etomidate on H2O2 induced PC12 cell injury

Objective To explore protective effect of etomidate on H2O2 induced PC12 cell injury. Methods PC12 cell was randomized into normal group, H2O2 group (200 μmol/L H2O2), etomidate low, medium and high-dose group. Cell viability, cell apoptotic rate, malondialdehyde (MDA) content, the activity of cysteinyl aspartate specific proteinase (Caspase)-3, Caspase-9, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), the expression of B-cell lymphoma-2 (bcl-2) and bcl-2 associated X protein (bax) was measured. Results Compared with normal group, cell viability [(0.38±0.03) vs. (0.65±0.06)] was decreased (P<0.01), the cell late apoptotic rate [(15.64±1.56)% vs. (2.32±0.23)%], cell late apoptotic rate [(24.61±2.46)% vs. (2.09±0.21)%], the activity of Caspase-3 [(4.39±0.44) vs. (0.58±0.05)], Caspase-9 [(2.95±0.29) vs. (0.48±0.04)], MDA content was increased (P<0.01), the activity of SOD, CAT and GSH-Px was decreased (P<0.01), the expression of bcl-2 was down-regulated (P<0.01), the expression of bax was up-regulated (P<0.01). Compared with H2O2 group, cell viability was increased (P<0.01), the cell apoptosis rate (P<0.01), the activity of Caspase-3 (P<0.01), Caspase-9 (P<0.01), MDA content was reduced (P<0.01), the activity of SOD (P<0.01), CAT (P<0.01) and GSH-Px (P<0.01) was increased, the expression of bcl-2 was up-regulated (P<0.01), the expression of bax was down-regulated (P<0.01). Conclusion Etomidate could suppress H2O2 induced PC12 cell injury via increasing antioxidant capacity and resistance to cell apoptosis. Key words: Etomidate; PC12 cell; H2O2; Injury