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连洪口调节FXR/TGR5/GLP-1途径以改善NAFLD小鼠的胰岛素抵抗:生物信息学和实验研究

Zhongyi Zhang^1,2, Yunliang He¹, Mei Zhao²

¹Institute of Traditional Chinese Medicine, Sichuan Academy of Chinese Medicine Sciences, Chengdu 610041, China.

|November 18, 2024

概括

青莲红 (Qinglian Hongqu) (QLHQD) 通过改善葡萄糖和脂质代谢,有效地治疗小鼠的非酒精性脂肪肝病 (NAFLD). 它的机制涉及激活FXR/TGR5/GLP-1通路,减少肝脂肪和胰岛素抵抗.

科学领域:

代谢性疾病研究研究.
传统中国医药传统中国医药
药理学药理学是指药理学的学科.

背景情况:

非酒精性脂肪性肝病 (NAFLD) 提出了重要的代谢挑战.
传统的中国草药药物,如青莲红 (QLHQD) ,显示出对NAFLD的治疗承诺.
需要阐明QLHQD对NAFLD影响的确切机制.

研究的目的:

在NAFLD小鼠模型中研究QLHQD的疗效.
探索QLHQD对NAFLD产生治疗作用的分子机制.
为了验证特定信号通路在QLHQD介导的NAFLD治疗中的作用.

主要方法:

建立了一个高脂肪饮食诱导的NAFLD小鼠模型.
评估了QLHQD对脂质和葡萄糖代谢标记物的影响.
使用网络药理学,生物信息学和分子对接来预测机制.
验证了关键蛋白质表达和途径目标,使用西式涂抹,免疫组织化学和qPCR.

主要成果:

在NAFLD小鼠中,QLHQD治疗显著改善了脂质概况,减少了肝肥胖症,并使葡萄糖耐受性和胰岛素耐药性正常化.
网络药理学表明胆酸分泌途径的参与.
实验验证证QLHQD调节FXR/TGR5/GLP-1信号通路,影响脂肪代谢和胰岛素敏感性.

结论:

在饮食诱导的NAFLD小鼠模型中,QLHQD在改善代谢功能障碍方面表现出显著的有效性.
QLHQD的治疗作用归因于肠道FXR/TGR5/GLP-1信号通路的激活.
这种途径的激活导致脂肪积累减少,并在NAFLD中改善胰岛素耐药性.

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