IngentaConnect Propofol attenuates oxidative stress-induced PC12 cell injury via...

Authors: WU, Xing-jun¹; ZHENG, Yong-jun²; CUI, Yong-yao¹; ZHU, Liang¹; LU, Yang; CHEN, Hong-zhuan

Source: Acta Pharmacologica Sinica, Volume 28, Number 8, August 2007 , pp. 1123-1128(6)

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-diphenyltetrazoliumbromide 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 μmol/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 PC 12 cell death through the inhibition of signaling pathways mediated by the p38 MAP kinase.

Keywords: propofol; oxidative stress; PC12 cells; apoptosis; p38 MAP kinase

Document Type: Research article

DOI: 10.1111/j.1745-7254.2007.00610.x

Affiliations: 1: Department of Pharmacy, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China 2: Department of Anesthesiology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200001, China

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