安菲瑞古林通过NF-κB和MAPK信号在肝炎中诱导iNOS和COX-2表达
Yu Jung Heo1,2, Nami Lee1, Sung-E Choi3
1Department of Endocrinology and Metabolism, Ajou University School of Medicine, 206, World cup-ro, Yeongtong-gu, Suwon 16499, Republic of Korea.
Mediators of inflammation
|October 23, 2023
概括
安菲瑞古林 (AREG) 通过通过NF-κB和MAPK信号通路增加氧化合成酶 (iNOS) 和循环氧化原酶-2 (COX-2) 来加剧非酒精性脂肪性肝病 (NAFLD) 的肝炎.
科学领域:
- 肝病学和免疫学 肝病学和免疫学
- 分子生物学分子生物学
背景情况:
- 肝炎是肝损伤和非酒精性脂肪性肝病 (NAFLD) 进展的关键驱动因素.
- 氨基素 (AREG) 是一种表皮生长因子受体连接体,与肝硬化和肝细胞癌有关.
研究的目的:
- 使用体内和体外模型研究NAFLD进展期间AREG在肝炎中的作用.
- 阐明AREG影响肝脏炎症通路的分子机制.
主要方法:
- 在甲胺胆缺乏 (MCD) 饮食下,在小鼠肝脏中分析了AREG基因表达.
- 用AREG刺激HepG2细胞以评估炎症介质 (NO,PGE2,IL-6,IL-1β,IL-8) 和信号通路 (NF-κB,MAPKs).
- 采用了酶相关的免疫吸收试验,西部涂抹和mRNA表达分析.
主要成果:
- 接受MCD饮食的小鼠在肝脏中增加了AREG表达,促炎细胞因子和免疫细胞标记物.
- 在HepG2细胞中AREG刺激增加了IL-6,IL-1β,NO,PGE2,并激活了iNOS和COX-2蛋白表达.
- AREG激活了NF-κB和MAPK信号通路,这些通路对AREG诱导的iNOS和COX-2表达至关重要.
结论:
- 在NAFLD中,AREG显著促进肝炎炎症.
- 通过激活NF-κB和MAPK信号通路,AREG促进了iNOS和COX-2的表达.
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