Cited by 10Alzheimer's disease research and treatmentsNeurological Disorders and TreatmentsMedicinal Plants and Neuroprotection

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

Su-fen, Yang, Zhong-jun, Wu, Zheng-qin, Yang, Qin, Wu, Qi-hai, Gong, Qi-xin, Zhou, Jing-shan, Shi·2005·Chinese Journal of Integrative Medicine

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.Conclusion 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.

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Crossref · 10.1007/bf02835792

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Authors
Su-fen, Y., Zhong-jun, W., Zheng-qin, Y., Qin, W., Qi-hai, G., Qi-xin, Z., & Jing-shan, S.
Affiliations
Chongqing Medical University (CN)
Venue
Chinese Journal of Integrative Medicine
Published
2005-12
Volume
11
Issue
4
Pages
293-296
ISSN
  • 1672-0415 (ISSN-L)
  • 1993-0402
OpenAlex
W2326186222
Cited by
10
References
12
Citations by year
2025: 2 · 2024: 1 · 2022: 2 · 2019: 1 · 2015: 1
FWCI
0.20
Type
journal article
Language
en
Open access
closed
Locations
  • Chinese Journal of Integrative Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
  • Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
Keywords
20-hydroxyecdysone, amyloid beta 25-35, PC12 cells, neuroprotection, cytotoxicity, oxidative stress, lipid peroxidation, malondialdehyde, superoxide dismutase, glutathione peroxidase, catalase, antioxidant enzymes, Alzheimer's disease, neurotoxicity, vitamin E, neuroprotection mechanism, neurodegeneration
MeSH terms
Animals, Catalase, Ecdysterone, Glutathione Peroxidase, L-Lactate Dehydrogenase, Malondialdehyde, Peptide Fragments, Amyloid beta-Peptides, PC12 Cells, Rats

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