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Updated: Jul 13, 2026
Exploring the Two Herb Combination Strategy to Treat Injured PC12 Cells
Published on: November 18, 2022
Propofol attenuates oxidative stress-induced PC12 cell injury via p38 MAP kinase dependent pathway
Xing-jun Wu1, Yong-jun Zheng, Yong-yao Cui
1Department of Pharmacy, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
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.
