Open AccessPropofol attenuates oxidative stress‐induced PC12 cell injury via p38 MAP kinase dependent pathway 1
Author(s) -
WU Xingjun,
ZHENG Yongjun,
CUI Yongyao,
ZHU Liang,
LU Yang,
CHEN Hongzhuan
Publication year - 2007
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2007.00610.x
Subject(s) - programmed cell death , p38 mitogen activated protein kinases , viability assay , kinase , microbiology and biotechnology , apoptosis , protein kinase a , mitogen activated protein kinase , chemistry , intracellular , signal transduction , biology , biochemistry
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 (H 2 O 2 )‐induced cell death and the inhibition of H 2 O 2 induced caspase‐3 activation and PC12 cell apoptosis. Propofol inhibited the H 2 O 2 ‐induced p38 MAP kinase, but not c‐Jun N‐terminal kinase or extracellular signal‐regulated kinase 1 and 2 activations. Conclusion: Propofol might attenuate H 2 O 2 ‐induced PC 12 cell death through the inhibition of signaling pathways mediated by the p38 MAP kinase.