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金色化物Rg1通过微RNA-152通过表观遗传调节Smad7在肝纤维化中的表达

Rongrong Zhang¹, Xinmiao Li¹, Yuxiang Gao¹

¹Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

Journal of ginseng research

|July 3, 2023

概括

银化物Rg1通过表观遗传抑制Smad7甲基化和上皮-介质细胞转换 (EMT) 来逆转肝纤维化. 这项研究通过miR-152/DNMT1途径澄清了Rg1的抗纤维性机制,提供了新的治疗见解.

科学领域:

肝病学肝病学是一种肝病学.
分子生物学分子生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

金生素Rg1 (Rg1) 是一种金生成分,具有抗炎,抗癌和肝保护作用.
在肝纤维化中,表皮-介质细胞过渡 (EMT) 对于肝星细胞 (HSC) 激活至关重要.
Rg1抗纤维作用的机制,特别是它对Smad7甲基化的影响,尚不清楚.

研究的目的:

调查Rg1在肝纤维化中的抗纤维性作用背后的机制.
确定Rg1对Smad7甲基化的影响及其在HSC激活中的作用.
探索微RNA-152 (miR-152) 和DNA甲基转移酶1 (DNMT1) 在Rg1的作用中的参与.

主要方法:

在体内 (四化碳模型) 和体内评估Rg1的抗纤维化作用.
分析了Smad7表达,Smad7甲基化和miR-152水平.
研究了DNMT1和miR-152/DNMT1轴在Rg1的机制中的作用.

主要成果:

Rg1显著降低了肝纤维化,原沉积和HSC增殖.
通过降低Desmin和增加E-cadherin,Rg1抑制了EMT.
由Rg1诱导的Smad7表达和脱甲基化,通过miR-152依赖的DNMT1.1抑制进行介导.

结论:

通过通过miR-152/DNMT1途径表观遗传调节Smad7表达,Rg1抑制HSC激活和肝纤维化.
Rg1通过抑制EMT,在一定程度上发挥抗纤维性作用.
这些发现阐明了Rg1对肝纤维化的治疗潜力.

关键词:

CCl4诱导的纤维化人参化物 Rg1 这就是米RNA.

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