Protective effect of ecdysterone on PC12 cells cytotoxicity induced by Beta-amyloid25–35

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Abstract
Objective: To examine the protective effect of ecdysterone (ECR) against beta-amyloid peptide fragment25–35 (Aß25–35)-induced PC12 cells cytotoxicity, and to further explore its mechanism.Methods: Experimental PC12 cells were divided into the Aß group (treated by Aß25–35 100 μmol/L), the blank group (untreated), the positive control group (treated by Vit E 100 μmol/L after induction) and the ECR treated groups (treated by ECR with different concentrations of 1, 50 and 100 μmol/L). The damaged and survival condition of PC12 cells in various groups was monitored by lactate dehydrogenase (LDH) release and MTT assay. The content of malondialdehyde (MDA) was measured by fluorometric assay to indicate the lipid peroxidation. And the antioxidant enzymes activities in PC12 cells, including Superoxide dismutases(SOD), catalase (CAT) and glutathione peroxidase(GSH-Px), were detected respectively.Results: After PC12 cells were treated with Aß25–35 (100 μmol/L) for 24 hrs, they revealed a great decrease in MTT absorbance and activity of antioxidant enzymes, including SOD, CAT and GSH-Px as well as a significant increase of LDH activity and MDA content in PC12 cells (P25–35 treatment, the above-mentioned cytotoxic effect of Aß25–35 could be significantly attenuated dose-dependently, for ECR 50 μmol/L,PP25–35 induced decrease of SOD and GSH-Px activity, but not on that of CAT.Conclusion: ECR could protect PC12 cells from cytotoxicity of Aß25–35, and the protective mechanism might be related to the increase of SOD and GSH-Px activities and the decrease of MDA resulting from the ECR-pretreatment.

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