在NAFLD中,硫素/葡萄素系统和肠道微生物群:相互作用,机制和治疗潜力
Minghui Zhu1, Omer M A Dagah1, Billton Bryson Silaa1
1Engineering Research Center of Coptis Development and Utilization/Key Laboratory of Luminescence Analysis and Molecular Sensing, Ministry of Education (Southwest University), College of Pharmaceutical Sciences, Southwest University, Chongqing 400715, China.
Antioxidants (Basel, Switzerland)
|September 28, 2023
概括
肠道微生物群的失衡通过影响肝脏的抗氧化系统,导致非酒精性脂肪性肝病 (NAFLD). 向肠道细菌和醇-氧化解酶通路可能提供新的NAFLD治疗方法.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 微生物学 微生物学
- 氧化压力研究研究 氧化压力研究
背景情况:
- 非酒精性脂肪性肝病 (NAFLD) 的发病包括氧化应激和肠道失调.
- 醇-氧化剂系统,包括甲素和甲素,在NAFLD中至关重要.
- 肠道失生症对肝脏醇-氧化剂系统的确切影响尚不清楚.
研究的目的:
- 审查细菌氧化应激在NAFLD中的作用.
- 阐明NAFLD中肠道失调和硫素介导的氧化还原调节之间的相互作用.
- 探索肠道微生物群代谢物如何通过依赖醇的氧化还原信号影响肝脏健康.
主要方法:
- 文献综述侧重于NAFLD,氧化应激,肠道微生物群和醇-氧化系统.
- 对将肠道微生物群失调与肝脏氧化还原平衡联系起来的机制的分析.
- 检查特定的细菌代谢物 (TMAO,LPS,SCFA等). 以及它们对肝脏通路的影响.
主要成果:
- 肠道失生症通过细菌诱导的氧化应激影响NAFLD.
- 微生物群衍生的代谢物 (TMAO,LPS,SCFA等) 调节肝脏炎症,脂质代谢和胰岛素抵抗.
- 这些代谢物通过依赖醇的氧化还原信号通路发挥作用.
结论:
- 肠道微生物群失生症在NAFLD中显著影响肝脏醇-redox系统.
- 对NAFLD的治疗策略应考虑肠道微生物群调节和醇-氧系统调节.
- 了解这种复杂的关系是新的NAFLD预防和治疗方法的关键.
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