阿托瓦斯塔丁通过AMPK/Mtor途径改善患有血管痴呆症的老鼠的认知缺陷
Xiuqin Li1,2, Shaopeng Chen3, Guiming Zheng4
1Department of Neurology, Hebei Medical University, Shijiazhuang, Hebei, 050017, China.
Combinatorial chemistry & high throughput screening
|June 7, 2023
概括
阿托瓦斯塔丁 (AC) 通过减少神经元损伤和激活AMPK/mTOR通路,保护神经细胞并改善血管痴呆 (VD) 模型中的认知功能.
科学领域:
- 神经科学是一个神经科学.
- 药理学 药理学是指药理学的学科.
- 细胞生物学 细胞生物学
背景情况:
- 血管性痴呆 (VD) 是一种神经退行性疾病,由于慢性大脑低,导致认知缺陷.
- 阿托瓦斯塔丁 (AC) 在治疗静脉疾病中的疗效和精确机制尚不清楚.
研究的目的:
- 为了研究AC对神经细胞和认知功能的保护作用,在体外和体内的体外VD模型.
- 阐明在早期风病中AC作用的潜在分子机制.
主要方法:
- 建立了体内 (2血管封闭) 和体内 (低氧/低氧化) 的静脉疾病模型.
- 使用莫里斯水迷宫评估空间学习和记忆.
- 分析了亡,自,氧化应激标志物和关键蛋白质表达 (Bax,LC3-II,Beclin-1,Bcl-2,AMPK/mTOR通路).
主要成果:
- AC减少了海马神经元和VD大鼠大脑中的亡,氧化应激和神经元损伤.
- 交流治疗改善了VD大鼠的认知功能,在莫里斯水迷宫中表现更好.
- AC调节了与亡/自相关的基因,并激活了AMPK/mTOR信号通路.
结论:
- 阿托瓦斯塔丁在静脉疾病模型中显示出神经保护作用.
- 通过调节亡/自和激活AMPK/mTOR通路,AC可能会缓解体内疾病中的认知缺陷和神经元损伤.
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