阿斯特拉加勒斯的多糖增强在炎症条件下通过肠道微生物群通过沃里康纳代谢
Xiaokang Wang1,2,3, Xianjing Hu2,4, Chunxiao Ye5
1The Marine Biomedical Research Institute of Guangdong Zhanjiang, Zhanjiang, Guangdong, China.
Journal of clinical and translational hepatology
|May 23, 2024
概括
阿斯特拉加卢斯多糖 (APS) 增强了沃里康纳 (VRC) 的新陈代谢,并通过增加Bifidobacterium bifidum,调节肠肝轴和CYP2C19表达来减少肝损伤.
科学领域:
- 药理学和毒理学 药理学和毒理学
- 微生物学和免疫学
- 肝病学 肝病学是一种肝病学.
背景情况:
- 沃里康纳 (VRC) 是一种关键的抗真菌剂,与显著的肝毒性有关.
- 阿斯特拉加勒斯多糖 (APS) 在调节VRC新陈代谢和减轻肝损伤方面显示出潜力.
- 在VRC新陈代谢中APS的确切机制尚待阐明.
研究的目的:
- 调查APS影响VRC代谢的潜在机制.
- 探索肠道微生物群,特别是Bifidobacterium bifidum在APS介导的VRC代谢调节中的作用.
- 通过肠肝轴确定APS对VRC诱导的肝毒性的影响.
主要方法:
- 使用罗塞尔·乌克拉夫因果关系评估方法尺度评估VRC-肝毒性关联.
- 在脂肪多糖诱导的老鼠炎症模型上进行了体外和体内实验.
- 使用了细胞因子分析,免疫组织化学,qPCR,代谢物分析,药物度测量,肠道生物多样性分析和Bifidobacterium bifidum补充.
主要成果:
- APS没有直接影响肝细胞,但显著增加了Bifidobacterium bifidum的丰富性.
- APS诱导了肝脏的抗炎反应,间接增强了VRC代谢.
- 通过NF-κB通路,APS抑制了促炎媒介分泌,并减少了通过NF-κB通路抑制CYP2C19转录的抑制.
结论:
- 通过对肝脏组织的免疫调节作用,APS可减轻VRC诱导的肝损伤.
- APS通过肠肝轴间接调节VRC代谢酶CYP2C19的表达.
- 这些发现突显了APS在管理与VRC相关的肝毒性方面的治疗潜力.
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