石杉碱甲对β-淀粉样蛋白（25-35）诱导的大鼠嗜铬细胞瘤细胞氧化损伤的保护作用。

Protective effects of huperzine A on beta-amyloid(25-35) induced oxidative injury in rat pheochromocytoma cells.

作者信息

Xiao X Q, Wang R, Han Y F, Tang X C

机构信息

State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 294 Tai-yuan Road, 200031, Shanghai, China.

出版信息

Neurosci Lett. 2000 Jun 9;286(3):155-8. doi: 10.1016/s0304-3940(00)01088-0.

DOI:10.1016/s0304-3940(00)01088-0

PMID:10832008

Abstract

The effects of huperzine A (HupA), a novel acetylcholinesterase inhibitor, on Abeta(25-35)-induced cell lesion, level of lipid peroxidation, antioxidant enzyme activities were investigated in the rat pheochromocytoma line PC12. Following a 48 h exposure of the cells to Abeta(25-35), a significant reduction in cell survival and activities of glutathione peroxidase (GSH-Px) and catalase (CAT), as well as increased production of malondialdehyde (MDA) and superoxide dismutase (SOD) were observed. Preincubation of the cells with HupA prior to Abeta(25-35) exposure elevated the cell survival and GSH-Px and CAT activities, and decreased the level of MDA and SOD activity. The results indicate that HupA has protective effects against Abeta-induced cell toxicity, which might be beneficial for the treatment of Alzheimer's disease.

摘要

石杉碱甲（HupA）是一种新型乙酰胆碱酯酶抑制剂，本研究在大鼠嗜铬细胞瘤细胞系PC12中探讨了其对β淀粉样蛋白（Aβ）（25 - 35）诱导的细胞损伤、脂质过氧化水平及抗氧化酶活性的影响。细胞经Aβ（25 - 35）处理48小时后，细胞存活率、谷胱甘肽过氧化物酶（GSH - Px）和过氧化氢酶（CAT）活性显著降低，丙二醛（MDA）和超氧化物歧化酶（SOD）生成增加。在Aβ（25 - 35）暴露前用HupA对细胞进行预孵育，可提高细胞存活率、GSH - Px和CAT活性，并降低MDA水平和SOD活性。结果表明，HupA对Aβ诱导的细胞毒性具有保护作用，这可能对阿尔茨海默病的治疗有益。