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硫化通过调节自而改善CUMS诱导的小鼠的类似抑郁的行为

Zhaoke Ling¹, Qingqing Kong², Zhiqiang He³

¹Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, Xuzhou, Jiangsu 221004, China; Department of Biophysics, School of Life Sciences, Xuzhou Medical University, Xuzhou, Jiangsu 221004, China.

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|March 2, 2025

概括

硫化 (H2S) 可能通过激活PI3K/AKT/mTOR通路,抑制自,并改善突触可塑性来治疗抑郁症. 持续的H2S治疗在小鼠中显示出显著的抗抑郁作用.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
药理学药理学是指药理学的学科.

背景情况:

抑郁症的发病包括突触损伤和破坏的自.
在抑郁症中观察到PI3K/AKT/mTOR信号传递和突触可塑性基因的表达减少.
硫化 (H2S) 通过增强突触可塑性,显示出神经系统疾病的潜力.

研究的目的:

为了研究H2S是否通过PI3K/AKT/mTOR信号调节自.
为了确定H2S是否能改善突触可塑性损伤,并产生抗抑郁作用.
为了阐明H2S的抗抑郁机制.

主要方法:

门德尔随机化 (MR) 分析确定了贝克林-1和抑郁风险之间的关联.
单细胞RNA测序 (scRNA-seq) 分析了抑郁症患者的神经元基因表达.
在小鼠中,慢性不可预测的轻度压力 (CUMS) 诱导了抑郁症,这些小鼠接受了H2S供体 (NaHS) 或PI3K抑制剂 (LY294002) 的治疗.

主要成果:

在小鼠中,CUMS诱导的抑郁症显示了p-PI3K,p-AKT,p-mTOR的减少,自的增加和突触可塑性受损.
NaHS治疗改善了类似抑郁症的行为,恢复了蛋白质表达,并增强了突触可塑性.
通过激活PI3K/AKT/mTOR信号,NaHS抑制了自,改善了突触可塑性缺陷.

结论:

通过激活PI3K/AKT/mTOR信号,抑制自和恢复突触可塑性,H2S显示出抗抑郁药的潜力.
持续的H2S治疗提供了更显著和持续的抗抑郁作用.
这项研究为治疗开发提供了对H2S抗抑郁机制的新见解.

关键词:

自自是一种自的过程.慢性不可预测的轻度压力硫化是一种硫化.突触性可塑性突触性可塑性

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