Propofol attenuates oxidative stress-induced PC12 cell injury via p38 MAP kinase dependent pathway

Abstract

Aim: To investigate the neuroprotective effect of propofol and its intracellular mechanism on neurons in vitro.

Methods: Cell viability was determined with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide reduction. Apoptotic cell death was determined by Hoechst 33258 staining and a fluorescence-activated cell sorter. The caspase-3 activity was measured by fluorometric assay. Mitogen-activated protein (MAP) kinase phosphorylation was detected with Western blotting.

Results: The pretreatment of rat pheochromocytoma cell line PC12 with propofol (1-10 micromol/L) resulted in a significant recovery from hydrogen peroxide (H2O2)-induced cell death and the inhibition of H2O2 induced caspase-3 activation and PC12 cell apoptosis. Propofol inhibited the H2O2-induced p38 MAP kinase, but not c-Jun N-terminal kinase or extracellular signal-regulated kinase 1 and 2 activations.

Conclusion: Propofol might attenuate H2O2-induced PC12 cell death through the inhibition of signaling pathways mediated by the p38 MAP kinase.