Abstract
Aim: To observe the effects of tanshinone IIA (Tan IIA) on the neurotoxicity induced by ethanol in PC12 cells and to explore its protective role. Methods: PC12 cell survival was measured by MTT assay. The formation of reactive oxygen species (ROS) and lactate dehydrogenase (LDH) release were detected by 2′,7′-dichlorofluorescin (DCF) fluorescence and calorimetric method, respectively. The percentage of cell apoptosis was monitored by flow cytometry. The expression of p53 was detected by immuno-fluorescence and flow cytometry. Results: Ethanol significantly impaired the survival of PC 12 cells as demonstrated by MTT assay. Ethanol also induced significant ROS formation and increased LDH release. Pre-incubation with Tan IIA in the culture medium significantly reversed these changes. Ethanol caused cell apoptosis and the upregulation of p53 protein. The anti-apoptosis effects of Tan IIA on ethanol-induced toxicity were accompanied by the downregulation of pro-apoptotic p53 protein expression. Conclusion: Tan IIA can protect neurons from apoptosis and might serve as a potential therapeutic drug for neurological disorders induced by ethanol. ©2006 CPS and SIMM.
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Meng, X. F., Zou, X. J., Peng, B., Shi, J., Guan, X. M., & Zhang, C. (2006). Inhibition of ethanol-induced toxicity by tanshinone IIA in PC12 cells. Acta Pharmacologica Sinica, 27(6), 659–664. https://doi.org/10.1111/j.1745-7254.2006.00324.x
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