美伐他汀降低β-淀粉样蛋白神经毒性的体外研究  

Study on mechanism of Mevastatin protection from neurotoxicity induced by amyliod-β

作　　者：黄美媚[1] 黎宏庄[1] 欧阳基鹏[1] 李国兴[1] 黎泳欣[1] 甘育鸿 Mei-mei Huang;Hong-zhuang Li;Ji-peng Ouyang;Guo-xing Li;Yong-xin Li;Yu-hong Gan(Department of Neurology,Shunde Hospital of Southern Medical University,Foshan,Guangdong 528300,China;Key Laboratory of Natural Medicine Research and Development,Guangdong Medical University,Zhanjiang,Guangdong 524023,China)

机构地区：[1]南方医科大学附属顺德第一人民医院神经内科,广东佛山528300 [2]广东医学院天然药物研究与开发重点实验室,广东湛江524023

出　　处：《中国现代医学杂志》2018年第14期31-34,共4页China Journal of Modern Medicine

摘　　要：目的通过美伐他汀降低β-淀粉样蛋白(Aβ)神经毒性,从机制角度探讨他汀类药物辅助治疗阿尔茨海默病的可能性。方法在实验室培养神经细胞,并加入美伐他汀,观察美伐他汀是否具有活化AMPK的能力,并观察在给予美伐他汀的同时,Aβ导致的过磷酸化现象是否得到抑制。结果在样品中加入美伐他汀时,人神经上皮瘤细胞(SK-N-MC)神经细胞数降低情况改善。Western blot检测结果发现,美伐他汀作用24 h后,SK-N-MC神经细胞AMPK磷酸化。结论美伐他汀可能通过提高AMPK活性,对抗Aβ导致的神经毒性,并进一步抑制蛋白质过磷酸化,发挥保护神经的作用。Objective To explore the possibility of Mevastatin treatment for Alzheimer's disease from the perspective of the mechanism of reducing amyloid-β(Aβ)neurotoxicity in vitro.Methods Neural cells were cultured in the laboratory and Mevastatin was added to observe whether Mevastatin could activate adenosine 5'-monophosphate(AMP)-activated protein kinase(AMPK),and the hyperphosphorylation induced by Aβcould be suppressed.Results Aβreduced the number of SK-N-MC,the situation was improved after adding Mevastatin.Western blot revealed phosphorylation of AMPK in the SK-N-MC after exposure to Mevastatin for 24 h.Conclusions We hypothesized that Mevastatin may be against the toxicity of beta-amyloid protein through enhancing the activity of AMPK,and further inhibit the phosphorylation of Tau to achieve its neuroprotective effect.

关 键 词：美伐他汀 阿尔茨海默病 Β-淀粉样蛋白 

分 类 号：R749.16[医药卫生—神经病学与精神病学]