通过TGR5/TPH1/5-HT激活,Pediococcus pentosaceus Li05对便秘的保护作用
Hui Chen1,2, Fengjiao Wang1, Shengjie Li1
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, Zhejiang, China.
Pediococcus pentosaceus Li05,是一种益生菌,通过调节胆酸代谢来缓解便秘. 这通过TGR5/TPH1通路增加了血清素 (5-HT) 水平,改善了肠道健康.
科学领域:
- 微生物学 微生物学
- 胃肠病学 胃肠病学
- 基因组学就是基因组学.
背景情况:
- Pediococcus pentosaceus Li05是一种乳酸细菌,具有潜在的健康益处.
- 便秘是一种常见的胃肠道疾病,具有复杂的病因.
- 肠道微生物群和胆酸代谢在调节胃肠功能方面发挥着至关重要的作用.
研究的目的:
- 为了描述Pediococcus pentosaceus Li05.05.的基因组.
- 调查Li05在小鼠中缓解洛佩拉胺诱导的便秘的机制.
- 探索胆酸代谢和TGR5/TPH1轴在Li05中介作用中的作用.
主要方法:
- 关于Pediococcus pentosaceus Li05.05的全基因组测序和生物信息分析
- 洛佩拉胺诱导的便秘小鼠模型.
- 分析肠道微生物组合,便胆盐化酶 (BSH) 活性和便胆酸概况.
- 测量结肠中的TGR5和TPH1表达和5-HT水平.
- 基因淘汰和药物抑制研究.
- 肠道有机体培养.肠道有机体培养.
主要成果:
- Li05基因组含有酸性基因,胆盐,氧化应激耐药性和粘附性,缺乏抗生素耐药性或毒性基因.
- 在小鼠中,Li05的使用改善了便秘症状,改变了肠道微生物群,增加了便的BSH活性,并改变了胆酸概况.
- Li05增加了结肠TGR5和TPH1的表达,导致5-HT水平升高,由TGR5淘汰或TPH1抑制逆转.
- 增加的胆酸 (DCA,Iso-LCA,EALCA) 通过肠道有机体中的TGR5/TPH1轴增强了5-HT水平.
结论:
- Pediococcus pentosaceus Li05 有效地缓解了便秘.
- 05通过调节胆汁酸代谢来发挥其有益作用.
- TGR5/TPH1信号通路,导致血清的产生增加,对于Li05在便秘中的治疗作用至关重要.
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