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拉贝普拉通过调节SMAD3链接区域酸化来减轻纤维化

Linkai Li¹, Zhen Liang¹, Long Fan¹

¹Department of Pharmacy, Zhuhai Center for Maternal and Child Health Care, Zhuhai, Guangdong 519000, P.R. China.

Biomedical reports

|December 22, 2025

概括

作为质子抑制剂的Rabéprazole通过抑制上皮层-介质细胞转换 (EMT) 来表现出抗纤维活性. 它上调TIF1γ,降低纤维蛋白和原蛋白,并与SMAD3相互作用以阻止纤维化信号传递.

科学领域:

细胞生物学细胞生物学
胃肠病学胃肠病学
药理学药理学是指药理学的学科.

背景情况:

皮质转介质过渡 (EMT) 和纤维化与TGFβ信号传递有关.
拉贝普拉是一种质子抑制剂 (PPI),用于*H. pylori*感染.
拉贝普拉的抗纤维作用尚不清楚.

研究的目的:

为了研究拉贝普拉的潜在抗纤维作用.
阐明拉贝普拉影响纤维化的机制.
检查拉贝普拉对胃上皮细胞EMT的影响.

主要方法:

西方涂抹和RT-qPCR用于基因表达分析 (mRNA和蛋白质).
免疫光,免疫沉 (IP) 和双 luciferase 记者测试来确定机制.
用于救援实验的等离子体转染.

主要成果:

拉贝普拉在AGS和GES-1细胞中抑制了EMT.
拉贝普拉上调调了转录介质因子1γ (TIF1γ) 的表达.
提升TIF1γ调节降低了纤维内素 (FN) 和原I型α1链 (Col1a1) 的表达.
拉贝普拉增强了TIF1γ和SMAD3之间的相互作用,抑制了SMAD3的酸化和核转位.

结论:

拉贝普拉表现出以前未知的抗纤维菌活性.
拉贝普拉的机制涉及TIF1γ上调和SMAD3相互作用.
这些发现扩大了拉贝普拉已知的生物功能,并揭示了一种新的抗纤维菌途径.

关键词:

SMAD家庭成员3 SMAD家庭成员3 纤维化纤维化链接酸化链接酸化转录中间因子1γ转录中间因子1γ

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