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

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。

Abstract:

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.