吉潘萨波基宁I通过向AKT1来减少炎症,并调节性结肠炎中的肠道微生物群
Mingyuan Yuan1, Bingxin Zhang1, Kexin Huang1
1School of Functional Food and Wine, Shenyang Pharmaceutical University, Shenyang, 110016, China.
Journal of ethnopharmacology
|January 6, 2026
概括
来自Gynostemma pentaphyllum的Gypensapogenin I (GI) 通过向AKT1并调节PI3K/AKT通路和肠道微生物群,有效治疗性结肠炎 (UC). 这项研究为UC提供了一种新的治疗策略.
科学领域:
- 药理学 药理学是指药理学的学科.
- 胃肠病学 胃肠病学
- 分子生物学分子生物学
背景情况:
- Gynostemma pentaphyllum (GP) 是一种传统的中国草药,对肠道疾病有着已知的作用.
- 来自GP的肥素Gypensapogenin I (GI) 显示出治疗性结肠炎 (UC) 的前景.
- 在UC治疗中GI的精确分子机制和点需要进一步阐明.
研究的目的:
- 系统地研究GI在UC中的治疗机制.
- 在UC中确定GI作用的分子点.
- 阐明GI对UC的作用所涉及的保护作用和途径.
主要方法:
- 已建立的硫酸 (DSS) 诱导的小鼠和脂聚糖 (LPS) 刺激的RAW264.7巨模型.
- 利用转录分析和16S rRNA测序来识别分子标并评估微生物群调制.
- 采用分子对接,SPR,CETSA,AKT1抑制剂和siAKT1实验来验证AKT1介导的PI3K/AKT通路.
主要成果:
- 胃肠道治疗显著延迟了UC的进展,并恢复了肠道屏障的完整性.
- 胃肠道通过PI3K/AKT通路减少了炎症反应和氧化应激.
- 胃肠道在调节微生物群-肠道-炎症轴方面发挥了治疗作用,主要是通过AKT1-介导的PI3K/AKT通路调节.
结论:
- GI通过准AKT1来调节PI3K/AKT通路和肠道微生物群来改善UC.
- 这些发现为开发GI作为新型UC治疗剂提供了理论基础.
- 胃肠道的机制包括调节肠道微生物群和炎症信号通路.
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