激活P2Y1R会阻碍肠道粘膜在结肠炎期间的修复
Qiuchan Huan1,2, Jiao Peng3, Yaoyao Chang1
1School of Pharmaceutical Sciences, Health Science Center, Shenzhen University, Shenzhen 518060, China.
International journal of biological sciences
|October 2, 2023
概括
腺二酸盐 (ADP) 激活P2Y1R,阻碍炎症性肠病 (IBD) 中的肠道愈合. 抑制P2Y1R促进了肠道修复,这表明它是IBD的治疗点.
科学领域:
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 肠粘膜愈合的延迟有助于炎症性肠病 (IBD) 的复发.
- 炎症损害肠道修复的机制尚未完全理解.
- 腺二酸盐 (ADP) 在炎症部位升高,并通过P2Y1R发出信号.
研究的目的:
- 研究ADP及其受体P2Y1R在炎症引起的肠粘膜损伤和修复中的作用.
- 探索P2Y1R作为IBD的潜在治疗点.
主要方法:
- 在性结肠炎 (UC) 患者和结肠炎小鼠模型中检查了P2Y1R表达.
- 使用TNF-α挑战的Caco-2细胞模型和P2Y1R淘汰 (P2Y1R-/-) 患有DSS诱导的大肠炎的小鼠.
- 研究了P2Y1R抑制对上皮质透性,伤口愈合,紧密结合完整性,AMPK酸化和肠道微生物群的影响.
主要成果:
- 在UC患者和大肠炎小鼠的结肠粘膜中,P2Y1R被上调.
- ADP/P2Y1R信号加剧了由炎症引起的上皮质屏障功能障碍和延迟的伤口愈合.
- 在大肠炎模型中,P2Y1R抑制改善了表皮屏障功能,增强了伤口愈合,促进了AMPK酸化,并恢复了肠道微生物群的稳态.
结论:
- 在大肠炎中,P2Y1R激活显著阻碍了肠粘膜的修复.
- 向P2Y1R代表了IBD治疗的有前途的治疗策略.
- 抑制P2Y1R通过调节上皮质完整性和微生物群来促进肠道修复.
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