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药物P以剂量依赖的方式减轻大鼠的脂聚糖引起的认知障碍

Prasada Chowdari Gurram¹, Suman Manandhar², Sairaj Satarker²

¹Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Manipal 576104, India; KL College of Pharmacy, Koneru Lakshmaiah Education Foundation, Green Fields, Vaddeswaram, Andhra Pradesh 522302, India.

|August 27, 2025

概括

在阿尔茨海默氏病 (AD) 模型中,物质P (SP) 显示了剂量依赖的作用. 低剂量的SP改善了认知功能并减少了神经炎症,而高剂量的SP并没有扭转这些缺陷.

科学领域:

神经科学
药理学
阿尔茨海默病的研究

背景情况:

神经炎症是阿尔茨海默病 (AD) 认知衰退的关键因素.
涉及P物质 (SP) 和其受体 (NK1R) 的神经素通路在AD中起作用,但其确切功能尚不清楚.
这需要对其剂量依赖的效果进行研究.

研究的目的:

在老鼠阿尔茨海默病模型中研究P (SP) 对脂聚糖 (LPS) 诱导的神经炎症和认知障碍的剂量依赖作用.
阐明SP-NK1R轴在AD病理生理学中的功能作用.

主要方法:

在老鼠体内注射脂多糖 (LPS) 诱导的阿尔茨海默病 (AD) 模型.
在21天内通过腹膜内注射两种不同剂量的物质P (SP) (50μg/ kg和500μg/ kg).
行为测试 (莫里斯水迷宫,新型物体识别,开放场地) 来评估认知和运动.
对脑组织中的炎症标记物 (TNF-α,IL-6),粉素β (Aβ),乙胆酶 (AChE),氧化应激标记物 (脂质过氧化,催化酶) 和CREB蛋白水平进行生物化学分析.

主要成果:

使用LPS显著诱导认知缺陷,增加神经炎症,粉素β (Aβ) 沉积,氧化应激和乙胆酶 (AChE) 活性,同时降低CREB蛋白水平.
较低剂量的SP (50μg/ kg) 有效地改善了认知障碍,并逆转了AD相关的病理标志物和神经炎症.
较高的SP剂量 (500μg/ kg) 对空间记忆或神经炎症没有显著的恢复作用,表明这种度缺乏有效性.

结论:

在阿尔茨海默病 (AD) 中,P (SP) 对神经炎症引起的认知缺陷具有剂量依赖的作用.
低剂量SP通过恢复认知功能和缓解AD病理表现出治疗潜力.
高剂量的SP在逆转认知障碍和神经炎症方面是无效的,这凸显了基于SP的AD治疗策略中剂量的至关重要.

关键词:

阿尔茨海默病脂聚糖类神经炎症神经素受体有关物质-P

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