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Inhibition of ethanol-induced toxicity by tanshinone IIA in PC12 cells

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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.

Keywords: PC12 cells; apoptosis; ethanol; p53; tanshinone IIA

Document Type: Research Article


Affiliations: 1: Department of Neurobiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China 2: Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

Publication date: June 1, 2006


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