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巴尔多克索隆甲基通过抑制巨细胞透来预防与代谢功能障碍相关的脂肪肝炎

Kazuhiro Onuma^1,2, Kenji Watanabe¹, Keishiro Isayama¹

¹Institute of Gene Research, Yamaguchi University Science Research Center, Yamaguchi, Japan.

British journal of pharmacology

|April 10, 2024

概括

巴尔多克索隆甲基 (CDDO-Me) 通过激活Nrf2并减少炎症性巨细胞透,有效地治疗小鼠的代谢功能障碍相关的脂肪肝炎 (MASH). 这项研究揭示了CDDO-Me.

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.
免疫学免疫学免疫学

背景情况:

代谢功能障碍相关的脂肪肝炎 (MASH) 是一个日益严重的健康问题,治疗选择有限.
巴多克索隆甲基 (CDDO-Me) 是已知的核因子红色素2相关因子2 (Nrf2) 的激活剂,在和肺炎性疾病中具有证明的保护作用.
对于MASH的CDDO-Me的治疗潜力,以肝脏脂肪积累为特征,此前尚未被探索.

研究的目的:

在饮食诱导MASH的小鼠模型中研究巴多克索隆甲基 (CDDO-Me) 的肝保护作用.
用RNA测序 (RNA-seq) 分析阐明CDDO-Me对MASH影响的药理机制.

主要方法:

给小鼠提供高脂肪饮食 (胆缺乏,L-氨基酸定义的高脂肪饮食) 来诱导MASH.
CDDO-Me被口服给MASH模型小鼠.
在肝脏组织上进行了组织学,生物化学和全转录组 (RNA-seq) 分析.

主要成果:

在小鼠中,CDDO-Me治疗显著改善了MASH症状.
转录组分析显示,CDDO-Me激活Nrf2通路,诱导抗氧化剂和胆固醇转运基因.
CDDO-Me抑制了炎症通路,特别是降低了巨细胞中CC化基因配体 (CCL3和CCL4) 和它们的受体 (CCR1和CCR5) 的表达,从而减少了巨细胞的透.

结论:

巴尔多克索隆甲基 (CDDO-Me) 在临床前小鼠模型中显示出对MASH的强烈肝保护作用.
治疗机制涉及Nrf2介导的抗氧化作用和通过CCL3-CCR1和CCL4-CCR5通路抑制炎症性巨细胞的招募.
这些发现强调了CDDO-Me作为MASH的有前途的治疗剂.

关键词:

CCL3 CCL3 CCL3 CCL3 CCL3 CCL3 CCL3 CCL3 CCL3 CCL3 CCL3 CCL4 CCL4 CCL4 CCL4 CCL4 CCL4 CCL4 CCL4 CCL4 CCL4 CCL4 CCL4 CCL4 CCL4 CCL4 CCL4 CCL4 CCL4 在CDDO-MeMe中.马什 (MASH) 是一个非常重要的产品.在RNA-seqq.巨细胞是一个巨细胞.

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