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Protective Effect of Ecdysterone on PC12Cells Cytotoxicity Induced by Beta-amyloid_(25-35) 被引量:3
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作者 杨素芬 吴忠均 +4 位作者 杨正钦 吴芹 龚其海 周岐新 石京山 《Chinese Journal of Integrated Traditional and Western Medicine》 2005年第4期293-296,共4页
Objective: To examine the protective effect of ecdysterone (ECR) against beta-amyloid peptide fragment25-35 (Aβ25-35)-induced PC12 cells cytotoxicity, and to further explore its mechanism. Methods: Experimental... Objective: To examine the protective effect of ecdysterone (ECR) against beta-amyloid peptide fragment25-35 (Aβ25-35)-induced PC12 cells cytotoxicity, and to further explore its mechanism. Methods: Experimental PC12 cells were divided into the Aβ group (treated by Aβ25-35 100μmol/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 Aβ25-35 (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 Aβ25-35 treatment, the above-mentioned cytotoxic effect of Aβ25-35 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 Aβ25-35 induced decrease of SOD and GSH-Px activity, but not on that of CAT. Conclusion: ECR could protect PC12 cells from cytotoxicity of Aβ25-35, 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. 展开更多
关键词 ECDYSTERONE beta-amyloid peptide fragment25-35 PC12 cells
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Fructus Broussonetae extract improves cognitive function and endoplasmic reticulum stress in Alzheimer's disease models 被引量:7
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作者 Yinghong Li Li Hu +6 位作者 Zhengzhi Wu Zhiling Yu Meiqun Cao Kehuan Sun Yu Jin Anmin Wu Andrew CJ Huang 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第30期2325-2331,共7页
This study investigated the effects and possible targets of Fructus Broussonetiae extract, a traditional Chinese medicinal herb, on a model of Alzheimer's disease induced by beta-amyloid peptide 25 35 and D-galactose... This study investigated the effects and possible targets of Fructus Broussonetiae extract, a traditional Chinese medicinal herb, on a model of Alzheimer's disease induced by beta-amyloid peptide 25 35 and D-galactose. The results revealed that intragastric administration of Fructus Broussonetiae significantly increased the expression of immunoglobulin-binding protein, a key factor in the endoplasmic reticulum stress-signaling pathway in rat hippocampus. In contrast, the treatment significantly decreased expression levels of PKR-like endoplasmic reticulum kinase and C/EBP homologous protein, and substantially improved learning, memory and spatial recognition dysfunction in rats. This evidence indicates that Fructus Broussonetiae extract improves spatial learning and memory abilities in rats by affecting the regulation of hippocampal endoplasmic reticulum stress and activation of the apoptosis pathway. 展开更多
关键词 Alzheimer's disease endoplasmic reticulum stress Fructus Broussonetiae extract beta-amyloid peptide 25-35 D-GALACTOSE RECOGNITION neural regeneration
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