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

Yang Su-fen; Wu Zhong-jun; Yang Zheng-qin; Wu Qin; Gong Qi-hai; Zhou Qi-xin; Shi Jing-shan

doi:10.1007/BF02835792

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

OriginalPaper | Updated：2021-08-27

- Protective effect of ecdysterone on PC12 cells cytotoxicity induced by Beta-amyloid25–35
- Protective effect of ecdysterone on PC12 cells cytotoxicity induced by Beta-amyloid25–35
- 中国结合医学杂志（英文版） 2005年11卷第4期页码：293-296
- Affiliations：
  
  1. Department of Pharmacology, Zunyi Medical College,Guizhou
  2. Department of Pharmacology, Chongqing Medical University,China
- Author bio：
- Funds：
  
  Supported by Governor Talent Foundation of Guizhou Province (No. 2001016)
- DOI：10.1007/BF02835792
  中图分类号：
- 纸质出版日期：2005，
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Su-fen, Y., Zhong-jun, W., Zheng-qin, Y. et al. Protective effect of ecdysterone on PC12 cells cytotoxicity induced by Beta-amyloid25–35, ., Chin. J. Integr. Med. 11, 293–296 (2005). https://doi.org/10.1007/BF02835792

Yang Su-fen, Wu Zhong-jun, Yang Zheng-qin, et al. Protective effect of ecdysterone on PC12 cells cytotoxicity induced by Beta-amyloid25–35[J]. Chinese Journal of Integrative Medicine, 2005,11(4):293-296.
Su-fen, Y., Zhong-jun, W., Zheng-qin, Y. et al. Protective effect of ecdysterone on PC12 cells cytotoxicity induced by Beta-amyloid25–35, ., Chin. J. Integr. Med. 11, 293–296 (2005). https://doi.org/10.1007/BF02835792 DOI：

Yang Su-fen, Wu Zhong-jun, Yang Zheng-qin, et al. Protective effect of ecdysterone on PC12 cells cytotoxicity induced by Beta-amyloid25–35[J]. Chinese Journal of Integrative Medicine, 2005,11(4):293-296. DOI： 10.1007/BF02835792.

摘要

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 (P<0.01). When the cells was pretreated with 1 – 100 μmol/L ECR for 24 hrs before Aß25–35 treatment

the above-mentioned cytotoxic effect of Aß25–35 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 Aß25–35 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.

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

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

the above-mentioned cytotoxic effect of Aß25–35 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 Aß25–35 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.

关键词

ecdysteronebeta-amyloid peptide fragment25–35PC12 cells

Keywords

ecdysteronebeta-amyloid peptide fragment25–35PC12 cells

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