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调节PI3K/AKT途径的表原蛋白改善了性大鼠的抑郁行为

Zhanfang Xie¹, Yang Zhao¹, Yanhong Wang¹

¹Department of Pharmacy, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.

Combinatorial chemistry & high throughput screening

|July 2, 2025

概括

原蛋白 (API) 通过保护海马神经元和星球细胞来减少性大鼠的和抑郁症. 这种黄胺激活PI3K/AKT通路,具有作为抗和抗抑郁药治疗的潜力.

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.

背景情况:

经常与抑郁症同时发生,从而降低了患者的生活质量.
海马在中很容易受到伤害,并与抑郁症和神经退行有关.
发生包括炎症,氧化应激和神经元损伤,PI3K/AKT通路至关重要.

研究的目的:

在引起的抑郁症的老鼠模型中研究阿皮基宁 (API) 的治疗机制.
专注于API对海马神经发生和PI3K/AKT信号通路的影响.
评估API作为抗和抗抑郁药物的潜力.

主要方法:

在使用化 (LiCl) 和皮洛卡尔的老鼠中诱导和抑郁症.
给药的API和氨酸 (VPA) 来评估对抑郁行为和星球细胞的影响.
利用网络药理学来预测API的的分子标.
进行了体内实验,以验证预测的机制.

主要成果:

API和VPA显著降低了发作频率,严重程度和抑郁行为.
组织学分析显示,API和VPA减轻了神经元损伤 (核收缩,细胞胀) 并改善了海马体结构 (尼斯尔体).
API和VPA逆转了PI3K/AKT通路信号的变化,并减少了状纤维酸蛋白 (GFAP) 表达,表明星细胞激活被抑制.

结论:

原蛋白 (API) 在老鼠模型中显示出抗和抗抑郁作用,与酸 (VPA) 相似.
通过调节PI3K/AKT通路,API减轻海马神经元损伤,并抑制星球细胞激活,这可能是通过调节PI3K/AKT通路.
作为治疗和并发性抑郁症的神经保护剂,API显得有前途,因此需要进一步研究其直接PI3K/AKT通路相互作用.

关键词:

是一种病.在PI3K/AKT中使用.它们的基因是apigenin.天体细胞.天体细胞.抑郁的行为抑郁的行为.

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