青花石颗粒通过调节Lactobacillus gasseri介导的铁代谢途径来改善实验性结肠炎
Cheng Cheng1, Lei Zhu2, Jingyi Hu2
1Jiangsu Province Engineering Research Center of TCM Health Preservation, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Chinese medicine
|January 25, 2026
概括
这项研究表明,QCHS通过抑制细胞死亡途径铁亡,缓解性结肠炎 (UC). 这些有益的效果是由Lactobacillus gasseri介导的,它被确定为一种新的铁灭抑制剂.
科学领域:
- 胃肠病学 胃肠病学
- 微生物学 微生物学
- 细胞生物学 细胞生物学
背景情况:
- 性结肠炎 (UC) 涉及上皮屏障功能障碍和炎症.
- 铁,一种依赖于铁的细胞死亡,以及肠道微生物群都与UC的病变产生有关.
- 目前的UC治疗由于复杂的病因而面临挑战.
研究的目的:
- 研究QCHS在性结肠炎 (UC) 的治疗潜力.
- 探索QCHS在调节铁亡和微生物群-代谢轴中的作用.
- 专门研究 Lactobacillus gasseri (L. gasseri) 在UC治疗中的功能.
主要方法:
- 利用DSS诱导的UC小鼠模型来评估QCHS的疗效.
- 使用16S rDNA测序和UHPLC-MS/MS.分析了肠道微生物群和代谢特征.
- 通过细胞模型和分子技术在体外研究L. gasseri的铁灭抑制.
主要成果:
- QCHS治疗显著降低了UC结肠组织中的铁亡.
- 牛乳杆菌被确定为一个关键的调解者和一种新的铁灭抑制剂.
- 在细胞模型中,L. gasseri通过激活GSH/GPX4通路来抑制铁亡.
结论:
- QCHS有效调节了UC中的微生物群-代谢轴和铁亡.
- 乳酸菌 (Lactobacillus gasseri) 在铁亡中发挥了一种新的抑制作用.
- 这些发现表明UC的潜在的微生物向和铁灭调节疗法.
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