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聚酸通过PPARγ/NF-κB信号通路调节炎症来减轻认知障碍

Tan Zhao¹, Jianping Jia^1,2,3,4,5

¹Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Beijing, China.

CNS neuroscience & therapeutics

|February 29, 2024

概括

来自Polygala tenuifolia的多甲酸 (PA) 可能通过减少炎症和保护神经元来治疗阿尔茨海默病 (AD). 研究表明,PA向PPARγ/NF-κB通路,提供了一个潜在的新治疗候选者.

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.
传统中国医药传统中国医药

背景情况:

阿尔茨海默病 (AD) 是一种进展性神经退行性疾病,其特点是认知能力下降和神经炎症.
传统中国医学 (TCM) 提供了潜在的治疗AD的化合物,包括来自Polygala tenuifolia的多酸 (PA).

研究的目的:

调查聚酸 (PA) 在阿尔茨海默氏症 (AD) 中的治疗潜力和分子机制.
探索PA在调节神经炎症和神经元亡中的作用.

主要方法:

网络药理学被用来预测PA的目标和途径.
用分子对接来评估PA与核心目标的结合亲和力.
在体内 (AD小鼠模型) 和体外 (微细胞和神经元共同培养) 进行了研究,以评估PA对炎症和亡的影响.

主要成果:

预计PA将准PPARγ介导的途径,可能调节炎症.
在体内研究表明,PA减轻了AD小鼠的认知缺陷,并减少了与炎症相关的因素.
实验室研究表明,PA降低了激活的微质细胞的炎症性细胞因子产生,并降低了神经元的亡,而PPARγ抑制剂 (GW9662) 则可以逆转效应.
在体外和体外模型中发现,PA通过PPARγ/NF-κB通路减轻炎症.

结论:

聚酸 (PA) 通过调节PPARγ / NF-κB通路并减少神经炎症,对阿尔茨海默病产生神经保护作用.
在阿尔茨海默氏症治疗中,PA显示出作为未来药物开发的有价值的治疗候选药物的潜力.

关键词:

阿尔茨海默病的疾病阿尔茨海默病的疾病.聚格拉酸是一种多酸.灭症 (apoptosis) 是一种死亡的过程.这是一种炎症炎症炎症炎症.

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