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沙利化物通过PPARγ介导的炎症信号通路缓解早期的MASH

Jun Zhang¹, Jintao Xuan², Zheyun He³

¹Liver Disease Department of Integrative Medicine, Ningbo No.2 Hospital, Ningbo, Zhejiang, 315010, China; Department of Infectious Diseases, Affiliated Hospital of Jiaxing University/The First Hospital of Jiaxing, Jiaxing, Zhejiang, 314000, China.

Journal of ethnopharmacology

|December 15, 2025

概括

化,源自Rhodiola rosea,通过激活PPARγ和抑制炎症,有效地治疗MASH. 这种天然化合物减少肝脏脂肪和炎症,为MASH提供了有前途的治疗途径.

科学领域:

药理学和传统医学的医学.
肝病学和代谢疾病
分子生物学和生物化学分子生物学和生物化学

背景情况:

罗迪奥拉 (Rhodiola rosea) 是一种以能量代谢和抗炎性质而闻名的传统草药.
它的活性成分沙利多化物显示出对MASH (代谢功能障碍相关的脂肪肝炎) 的保护潜力.
在MASH中沙利德胺的确切作用机制尚未完全理解.

研究的目的:

在MASH的小鼠模型中评估salidroside的治疗疗效.
阐明沙利德胺对MASH的保护作用的潜在分子机制.

主要方法:

在使用CDAHFD (胆缺乏氨基酸定义的高脂肪饮食) 的小鼠中诱导MASH.
小鼠接受了四周的沙利德化物治疗,随后进行了包括多组学,网络药理学和分子对接在内的综合分析.
通过使用特定抑制剂GW9662.2,证实了PPARγ的作用.

主要成果:

化治疗显著降低了肝脂积累,肝损伤标志物 (ALT,AST) 和MASH分数.
转录组和代谢组数据表明PPAR信号通路的激活,PPARγ被确定为关键目标.
沙利德胺提高了PPARγ的调节,抑制了NF-κB酸化,并减少了促炎性细胞因子,GW9662消除了这些效应.

结论:

沙利化物通过激活PPARγ通路并抑制NF-κB炎症级联来缓解MASH.
这种机制导致肝脏脂质沉积和炎症的减少,突出显示了salidroside对MASH的治疗潜力.

关键词:

马什 (MASH) 是一个非常重要的产品.这就是NF-κBB.在PPARγ中,PPARγ是PPARγ 沙利德化物是一种化物.

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