情绪稳定剂 (拉莫特里金,和瓦尔酸) 通过抑制神经细胞中TRPM2通道,减少双极性疾病模型 (Ouabain) 诱导的氧化应激和亡

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Updated: Jan 17, 2026

04:42

Developing a Rat Model for Bipolar Disorder

Published on: May 2, 2025

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Esra Nur Kaplan¹, İbrahim Eren¹, Mustafa Nazıroğlu^2,3,4

¹Department of Psychiatry, Faculty of Medicine, Suleyman Demirel University, Isparta, Türkiye.

Bipolar disorders

|September 19, 2025

概括

情绪稳定剂,酸和拉莫特里金通过抑制TRPM2通道来保护双极性疾病 (BD) 神经毒性. 这些治疗方法减少了氧化应激,亡和流入,为BD提供了潜在的治疗益处.

科学领域:

神经科学是一个神经科学.
细胞生物学细胞生物学
药理学药理学是指药理学的学科.

背景情况:

双极性疾病 (BD) 与线粒体反应性氧物种 (mROS),亡和 (Ca2+) 流入有关.
通过mROS激活TRPM2通道有助于神经系统疾病中的神经元死亡,包括潜在的BD.
像lamotrigine (LMT), (Li) 和酸 (VPA) 这样的情绪稳定剂具有抗氧化特性,但它们通过BD中TRPM2抑制的神经保护机制尚不清楚.

研究的目的:

研究LMT,Li和VPA对SH-SY5Y神经细胞中ouabain (OUA) 诱导的氧化神经毒性的神经保护作用.
确定这些保护措施是否涉及TRPM2通道的调制.

主要方法:

用OUA,LMT,Li,VPA或它们的组合对待SH-SY5Y神经细胞.
评估了TRPM2通道活性,mROS产生,细胞质ROS,脂质过氧化,线粒体膜潜力,亡标记物 (caspase-3, -8, -9),Zn2+水平和细胞活力.
使用TRPM2抗剂来确认通道参与.

主要成果:

对OUA的暴露增加了TRPM2活性,mROS,ROS,脂质过氧化,亡,Zn2+和细胞死亡.
LMT,Li和VPA治疗,以及TRPM2抗剂,显著降低了OUA诱导的TRPM2刺激和电流密度.
这些情绪稳定剂还减少了OUA诱导的氧化应激和亡标志物,同时增加了细胞活力和抗氧化防御 (谷,谷过氧化酶).

结论:

LMT,Li和VPA有效调节OUA诱导的氧化应激,亡,Zn2+水平和谷氨通路.
这些情绪稳定剂抑制TRPM2介导的Ca2+过量流入,这表明它们在BD中的神经保护的关键机制.
这些发现突显了这些药物的潜力,用于治疗与高mROS,Ca2+和Zn2+相关的BD.

关键词:

TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2TRPM2 灭症 (apoptosis) 是一种死亡的过程.双相情感障碍双相情感障碍双相情感障碍黑激素是什么意思黑激素是什么意思情绪稳定剂情绪稳定剂氧化应激是一种氧化应激.

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