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塞达诺利德通过调节小鼠的肠道FXR-SMPD3通路来缓解DSS诱导的大肠炎

Shengjie Li¹, Aoxiang Zhuge¹, Hui Chen¹

¹State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, National Medical Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.

Journal of advanced research

|April 6, 2024

概括

塞达诺利德通过调节肠道微生物群和胆酸代谢来有效治疗炎症性肠道疾病 (IBD),最终减少炎症并恢复肠道屏障功能.

科学领域:

胃肠病学胃肠病学
微生物学微生物学
代谢学代谢学代谢学

背景情况:

炎症性肠病 (IBD) 是一个全球性的健康挑战,治疗选择有限.
塞达诺利德是一种天然的甲基,具有已知的抗氧化和抗炎性质,但其在IBD中的有效性仍然未被探索.

研究的目的:

为了调查sedanolide在硫酸 (DSS) 诱导的大肠炎中的治疗潜力,IBD的小鼠模型.
阐明塞达诺利德对肠道炎症,屏障功能和肠道微生物群的影响背后的机制.

主要方法:

小鼠接受了类或载体治疗,随后给予DSS诱导大肠炎.
评估大肠炎的严重程度,炎症标志物和肠道屏障完整性.
进行了转录组,16S rRNA测序和胆酸和脂质的向代谢分析.

主要成果:

西达诺利德的使用显著地保护了DSS诱导的大肠炎,减少了炎症并恢复了上皮屏障功能.
塞达诺利德改变了肠道微生物群的组成,减少了表达胆盐酸酶 (BSH) 的细菌,这些细菌调节胆酸特征,并抑制了farnesoid X受体 (FXR) 途径.
确定了胺 (d18:1/16:0) 作为一个关键的调解剂,其合成是由sedanolide对FXR-SMPD3通路的抑制刺激的,在体外证明了保护作用.

结论:

塞达诺利德重塑肠道微生物组和胆汁酸组成,抑制FXR-SMPD3通路以促进胺合成,从而减轻DSS诱导的大肠炎.
这些发现表明sedanolide作为潜在的临床治疗大肠炎.
这项研究强调了胺作为一种关键的脂质代谢物,它调解了sedanolide在结肠炎中的保护作用.

关键词:

胆汁酸代谢胆汁酸代谢陶化物陶化物大肠炎是什么意思在 FXR 和 FXR 之间.肠道微生物肠道微生物这是一种Sedanolide.

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