阿斯特拉加卢斯多糖胺通过一种依赖于酸受体的自机制保护实验性结肠炎
Yi Ying1,2, Li-Yun Song1, Wen-Lin Pang1
1Yunnan Provincial Key Laboratory of Integrated Traditional Chinese and Western Medicine for Chronic Disease in Prevention and Treatment, Yunnan University of Chinese Medicine, Kunming, Yunnan, China.
British journal of pharmacology
|September 1, 2023
概括
阿斯特拉加卢斯多糖 (APS) 通过激活酸受体 (AhR) 来保护大肠炎,以促进自和修复肠道屏障. 这种机制对于维持肠道健康和减少炎症至关重要.
科学领域:
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
- 药理学 药理学是指药理学的学科.
背景情况:
- 肠道屏障的破坏是大肠炎发病的核心原因.
- 亚利碳化合物受体 (AhR) 调节肠道免疫恒温和炎症.
- 阿斯特拉加卢斯多糖 (APS) 显示在结肠炎中具有治疗潜力,但其机制尚不清楚.
研究的目的:
- 为了调查APS是否通过AhR-依赖的自来保护大肠炎.
- 阐明在结肠炎中APS治疗效果背后的分子机制.
主要方法:
- 在接受APS治疗的小鼠中评估了DSS诱导的大肠炎.
- 使用了肠道特异性Becn1条件淘汰 (Becn1 cKO) 鼠标.
- 使用记者测定和ChIP-qPCR评估了自,AhR失活效应和AhR-Becn1相互作用.
- 在Caco-2细胞中研究了炎症反应和自.
主要成果:
- 在大肠炎模型中,APS改善了肠道屏障功能,并减少了炎症损伤.
- 由APS诱导的自取决于AhR的表达.
- 激活的AhR与Becn1促进体结合,增强抗炎和障碍修复基因转录.
- 成为1淘汰赛加剧大肠炎,减少APS的疗效.
结论:
- 通过AhR激活,APS通过向自细胞来保护大肠炎.
- 通过APS刺激AhR促进肠道屏障的修复,并具有抗炎作用.
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