酸通过调节IL17 - NFκB和微生物群 - 甲基化通路来保护大肠炎
Minghui Wang1, Xiaoxuan Xu2, Mingxuan Sheng3
1Department of Animal Science & Technology, Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Agricultural University, Shandong 271018, China.
酸通过减少炎症和改变肠道细菌来预防结肠炎,显示出有前途. 它可能通过抑制IL-17-NF-κB通路并促进有益的甲基化过程而起作用.
科学领域:
- * 胃肠道学和免疫学
- * 营养科学和微生物学
背景情况:
- * 酸是一种来自植物的多,因其抗炎性质而受到研究.
- * 它在预防大肠炎方面的潜力需要进一步研究机制和疗效.
研究的目的:
- * 在小鼠模型中评估酸的抗结肠炎作用.
- * 阐明酸作用的基础分子和微生物机制.
主要方法:
- * 在小鼠中对酸 (0-3毫克/毫升) 的剂量范围研究.
- * DSS诱导的大肠炎模型,以评估治疗效果.
- *对IL-17-NF-κB信号传递,表观遗传修饰和肠道微生物群组成的分析.
主要成果:
- * 酸 (3毫克/毫升) 缓解了结肠炎症状.
- *观察到IL-17-NF-κB通路的抑制和甲基化通路的调节.
- * 丹尼酸增加了有益的肠道细菌 (Prevotella,Eubacterium_siraeum_group,Enterorhabdus). 这种细菌可以在肠道中生长.
- * Eubacterium siraeum补充剂也减少了结肠炎和增加了叶酸/甲基化调节剂.
结论:
- * 酸显示出作为抗结肠炎剂的潜力.
- * 机制包括抑制IL-17-NF-κB信号传递和增强微生物群驱动的甲基化.
- *肠道微生物群的调节,特别是由Eubacterium siraeum发挥着关键作用.
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