暴露于Cu会通过调节肠道微生物群/LPS/肝脏TLR4信号轴诱导肝炎
Tiantian Gu1, Minghua Kong2, Mingcai Duan1
1State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, China; Institute of Animal Husbandry and Veterinary Science, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, China; Key Laboratory of Livestock and Poultry Resources (Poultry) Evaluation and Utilization, Ministry of Agriculture and Rural Affairs of China, Hangzhou, 310021, China; Zhejiang Key Laboratory of Livestock and Poultry Breeding, Hangzhou 310021, China; Zhejiang Provincial Engineering Research Center for Poultry Breeding Industry and Green Farming Technology, Hangzhou 310021, China.
过度接触铜会通过破坏肠道微生物群和破坏肠道屏障,导致子肝炎. 便微生物种移植证实了肠肝轴在铜诱导的肝毒性中的作用.
科学领域:
- 动物科学动物科学
- 毒理学 毒理学 毒理学
- 胃肠病学 胃肠病学
背景情况:
- 铜 (Cu) 是必不可少的,但在高水平上是有毒的,导致肝炎.
- 肠肝轴在Cu诱导的肝毒性中的作用尚未完全理解.
研究的目的:
- 通过肠肝轴,研究暴露如何影响子肝炎.
- 为了确定肠道微生物群和屏障功能中的特定变化.
主要方法:
- 评估肝酶 (AST,ALT) 和炎症类细胞因子 (IL-1β,IL-6,TNF-α).
- 分析了肠道微生物群的组成和肠道屏障蛋白的表达 (Occludin,Claudin-1,ZO-1).
- 进行了便微生物群移植 (FMT) 实验.
主要成果:
- 通过LPS/TLR4/NF-κB通路,Cu暴露增加了肝酶和促炎细胞因子.
- 改变了肠道菌群,增加了有害细菌,减少了有益的细菌,如乳酸菌.
- Cu损害了肠道屏障,减少了屏障蛋白的表达,并增加了肠道炎症.
结论:
- 暴露于Cu会通过破坏肠肝轴来诱导子的肝炎.
- 肠道微生物群失调和肠道屏障功能受损是中Cu诱导的肝毒性的主要机制.
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