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 Aβ could be suppressed. Results Aβ reduced 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.%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.
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