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西诺因通过阻断TGF-β/SMAD和c-JUN信号传递来改善肝纤维化

Yichao Du^1,2, Junjie Bai³, Tingting Ma⁴

¹Department of Gastroenterology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, People's Republic of China.

Phytotherapy research : PTR

|June 1, 2025

概括

西诺因 (SIN) 通过抑制关键信号通路,有效治疗肝纤维化. 这种传统中医药化合物显示出作为慢性肝损伤的新疗法具有前景.

科学领域:

药理学药理学是指药理学的学科.
肝病学肝病学是一种肝病学.
分子生物学分子生物学

背景情况:

肝纤维化是慢性肝损伤的严重后果,治疗选择有限.
传统中医药中一种类化合物Sinomenine (SIN) 已显示出各种药理作用,但其抗纤维化机制尚不清楚.

研究的目的:

为了研究Sinomenine (SIN) 的抗纤维效应.
阐明SIN在肝纤维化中的潜在分子机制.

主要方法:

在碳四化物 (CCl4) 和胆道结合 (BDL) 诱导的小鼠肝纤维化模型中评估了SIN疗效.
使用转化生长因子β1 (TGF-β1) 刺激的老鼠肝细胞 (HSC-T6) 的体外研究.
通过生物化学标志物,组织病理学,免疫光学和西部斑点来评估肝损伤和纤维化,以分析信号通路.

主要成果:

在体内和体外,SIN显著降低了肝损伤和纤维化标志物.
SIN抑制了原沉积,并降低了α-平滑肌动蛋白 (α-SMA),MMP2和原I的调节.
通过降低SMAD2/3酸化,SIN抑制了TGF-β/SMAD通路,并通过降低p-c-JUN水平减弱了c-JUN信号传递.

结论:

西诺因 (SIN) 通过抑制TGF-β/SMAD和c-JUN信号通路来改善肝纤维化.
SIN显示出作为治疗肝纤维性疾病的治疗剂的潜力.

关键词:

这就是"sinomenine".在TGF-β/SMAD中使用.c-JUN 月日.肝脏纤维化肝脏纤维化

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