title: Protective effect of ecdysterone on PC12 cells cytotoxicity induced by beta-amyloid25-35.
abstract: OBJECTIVE
  To examine the protective effect of ecdysterone (ECR) against beta-amyloid peptide fragment(25-35) (Abeta(25-35))-induced PC12 cells cytotoxicity, and to further explore its mechanism.
  
  
  METHODS
  Experimental PC12 cells were divided into the Abeta group (treated by Abeta(25-35) 100 micromol/L), the blank group (untreated), the positive control group (treated by Vit E 100 micromol/L after induction) and the ECR treated groups (treated by ECR with different concentrations of 1, 50 and 100 micromol/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 Abeta(25-35) (100 micromol/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 micromol/L ECR for 24 hrs before Abeta(25-35) treatment, the above-mentioned cytotoxic effect of Abeta(25-35) could be significantly attenuated dose-dependently, for ECR 50 micromol/L, P < 0.05 and for ECR 100 micromol/L, P < 0.01. Moreover, ECR also showed significant inhibition on the Abeta(25-35) induced decrease of SOD and GSH-Px activity, but not on that of CAT.
  
  
  CONCLUSIONS
  ECR could protect PC12 cells from cytotoxicity of Abeta(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.
authors.affiliation: Department of Pharmacology, Zunyi Medical College, Guizhou 563003.
authors.forename: Su-fen
authors.initials: SF
authors.lastname: Yang
authors.forename: Zhong-jun
authors.initials: ZJ
authors.lastname: Wu
authors.forename: Zheng-qin
authors.initials: ZQ
authors.lastname: Yang
authors.forename: Qin
authors.initials: Q
authors.lastname: Wu
authors.forename: Qi-hai
authors.initials: QH
authors.lastname: Gong
authors.forename: Qi-xin
authors.initials: QX
authors.lastname: Zhou
authors.forename: Jing-shan
authors.initials: JS
authors.lastname: Shi
mesh_terms: D016229:Amyloid beta-Peptides / Q000633:toxicity*; D000818:Animals; D002374:Catalase / Q000032:analysis; D004441:Ecdysterone / Q000494:pharmacology*; D005979:Glutathione Peroxidase / Q000032:analysis; D007770:L-Lactate Dehydrogenase / Q000032:analysis; D008315:Malondialdehyde / Q000032:analysis; D016716:PC12 Cells; D010446:Peptide Fragments / Q000633:toxicity*; D051381:Rats
chemical_list: D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C074636:amyloid beta-protein (25-35); D008315:Malondialdehyde; D004441:Ecdysterone; D007770:L-Lactate Dehydrogenase; D002374:Catalase; D005979:Glutathione Peroxidase