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Objective: To examine the protective effect of ecdysterone (ECR) against beta-amyloid peptide fragment_ 25-35 (Aβ_ 25-35 )-induced PC12 cells cytotoxicity, and to further explore its mechanism.Methods: Experimental PC12 cells were divided into the Aβ group (treated by Aβ_ 25-35 100 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 Aβ_ 25-35 (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 (P<0.01). When the cells was pretreated with 1-100 μmol/L ECR for 24 hrs before Aβ_ 25-35 treatment, the above-mentioned cytotoxic effect of Aβ_ 25-35 could be significantly attenuated dose-dependently, for ECR 50 μmol/L, P<0.05 and for ECR 100 μmol/L, P<0.01. Moreover, ECR also showed significant inhibition on the Aβ_ 25-35 induced decrease of SOD and GSH-Px activity, but not on that of CAT. Conclusion: ECR could protect PC12 cells from cytotoxicity of Aβ_ 25-35 , 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.
Objective: To examine the protective effect of ecdysterone (ECR) against beta-amyloid peptide fragment_ 25-35 (Aβ_25-35) -induced PC12 cells cytotoxicity, and to further explore its mechanism. Methods: Experimental PC12 cells were divided into Aβ (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 Aβ_25-35 / L) for 24 hrs, they re vealed 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 (P <0.01). When the cells were pretreated with 1- 100 μmol / L ECR for 24 hrs before Aβ_ 25-35 treatment, the above-mentioned cytotoxic effect of Aβ_25-35 could be significantly attenuated dose-dependently, for ECR 50 μmol / L, P <0.05 and for ECR 100 μmol / L, P <0.01. ECR also showed significant inhibition on the Aβ_25-35 induced decrease of SOD and GSH-Px activity, but not on that of CAT. Conclusion: ECR could protect PC12 cells from cytotoxicity of Aβ_25-35 , 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.