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贝塔希斯对脂聚糖诱导的神经毒性的神经保护作用:实验和计算研究的见解

Vasudevan Mani¹, Minhajul Arfeen²

¹Department of Pharmacology and Toxicology, College of Pharmacy, Qassim University, Buraydah 51452, Saudi Arabia.

|September 28, 2024

概括

贝塔希斯 (BHTE) 通过减少神经炎症,氧化应激和亡来保护神经毒性. 这种组胺H3受体对手可以改善认知功能,并为治疗神经退行性疾病提供潜力.

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.
生物化学生物化学

背景情况:

组胺H3受体 (H3R) 抗剂,如贝塔希斯 (BHTE),在中枢神经系统 (CNS) 疾病中表现有前途.
神经炎症和神经退行是LPS诱导的神经毒性的关键特征.

研究的目的:

研究BHTE对大鼠中脂聚糖 (LPS) 诱导的神经毒性的神经保护作用.
评估BHTE对认知功能,神经炎症,氧化应激,线粒体功能障碍和亡的影响.

主要方法:

在LPS注射前30天,老鼠接受了BHTE (5或10毫克/公斤) 的预治疗.
用迷宫测试来评估认知表现.
神经炎症,氧化应激,线粒体功能和亡标志物被生物化学测量.
用分子建模来研究BHTE与向酶的结合.

主要成果:

LPS诱导认知障碍,降低乙胆 (ACh) 水平,增加神经炎症,氧化应激,线粒体功能障碍和亡.
在BHTE前期治疗改善了认知表现,并恢复了ACh水平.
BHTE显著降低了促炎性标记物 (COX-2,TNF-α,IL-6) 和亡标记物 (caspase-3),同时增强了抗炎性细胞因子 (IL-10,TGF-β1).
BHTE改善了线粒体功能和抗氧化剂防御 (GSH,催化酶),并降低了MDA水平.
分子建模证实了BHTE与ACHE,COX-2和caspase-3的结合.

结论:

贝塔希斯对LPS诱导的神经毒性产生显著的神经保护作用.
BHTE可以缓解神经炎症,氧化应激,线粒体功能障碍和亡.
BHTE显示出作为神经炎症和神经退行性疾病的治疗剂的潜力.

关键词:

抗氧化剂抗氧化剂是一种抗氧化剂.灭症 (apoptosis) 是一种死亡的过程.贝塔希斯类药物 (betahistine) 是一种认知功能认知功能脂多糖类糖化物 (Lipopolysaccharide) 是一种脂多糖类糖.线粒体中的线粒体.分子对接模拟分子对接模拟神经炎症是一种神经炎症.

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