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通过MAPK信号通路,ADAM8促进酒精性肝纤维化

Mengli Yang^1,2, Sanqiang Li^3,4, Renli Luo^1,2

¹The Molecular Medicine Key Laboratory of Liver Injury and Repair, College of Basic Medicine and Forensic Medicine, Henan University of Science and Technology, 263 KaiYuan Road, Luoyang, 471000, Henan, China.

The journal of physiological sciences : JPS

|October 15, 2024

概括

一个分解蛋白和金属蛋白酶8 (ADAM8) 通过激活MAPK信号通路来促进酒精性肝纤维化 (ALF). 抑制ADAM8显示出治疗ALF.的前景.

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
生物化学生物化学

背景情况:

酒精性肝纤维化 (ALF) 是一个重要的健康问题,具有复杂的分子机制.
解体蛋白和金属蛋白酶8 (ADAM8) 已与纤维性疾病有关,但其在ALF中的作用需要进一步阐明.

研究的目的:

研究ALF中ADAM8的作用和分子调节机制.
探索ADAM8作为ALF的潜在治疗点.

主要方法:

在C57BL/6N小鼠和LX-2人类肝星细胞中建立ALF模型.
在体内和体外实验中使用ADAM8-sgRNA3等离子体和si-ADAM8转染.
分析ADAM8表达,肝纤维化标志物和MAPK信号通路激活,通过血清检测,病理染色,西部斑点,qRT-PCR和CCK8测定.

主要成果:

抑制ADAM8 (使用ADAM8-sgRNA3等离子体 in vivo和si-ADAM8 in vitro) 显著降低了肝纤维化指标,病理变化和ADAM8的表达.
抑制ADAM8导致肝纤维化关键标志物的表达减少,并抑制了MAPK信号通路的激活 (包括p-ERK1/2,p-p38MAPK).
在si-ADAM8组中,细胞活力下降,这表明ADAM8.8具有亲纤维作用.

结论:

ADAM8在促进ALF中发挥着至关重要的作用,主要是通过激活MAPK信号通路.
向ADAM8为治疗酒精性肝纤维化提供了一个有前途的治疗策略.

关键词:

在 ADAM8 中,酒精性肝脏纤维化是什么肝脏的星状细胞是什么在 MAPK 信号通道中.

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