增加的肠道透性和脂多糖类化合物有助于斯万森因引起的全身炎症
Ling Lei1, Dazhi Deng2, Wenqian Xu3
1Clinical Psychology, Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region, Guangxi Key Laboratory of Reproductive Health and Birth Defect Prevention, Nanning, China.
Ecotoxicology and environmental safety
|August 24, 2024
概括
斯旺森因是一种毒素,增加了肠道的透性和脂多糖化物 (LPS) 水平. 这会引发全身炎症,为牲畜中毒机制提供新的见解.
科学领域:
- 毒理学 毒理学 毒理学
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
背景情况:
- 斯旺森因是一种已知的畜牧毒素,通过亡和自功能受损导致肝损伤.
- 斯瓦宁素诱导的全身炎症背后的精确机制,特别是它对肠道的影响,尚未完全理解.
研究的目的:
- 调查斯万森因对肠道透性,脂多糖 (LPS) 水平和氧化应激的影响.
- 为了阐明肠道屏障功能和LPS在斯瓦宁素毒性中的作用.
主要方法:
- 治疗小鼠的swainsonine,以评估变化结肠杯细胞,Akkermansia muciniphila,和紧密结合蛋白 (Occludin,克劳丁1,ZO-1).
- 肠道透性指标Ptprh的mRNA表达在阴茎中被分析.
- 肠道微生物群LPS生物合成基因和血液LPS水平被量化.
主要成果:
- 斯旺森因显著减少了杯状细胞,Akkermansia muciniphila和紧结蛋白,表明肠道透性增加.
- 升高的LPS生物合成基因和增加的肠道透性导致更高的血液LPS水平.
- 高LPS度诱导了促炎性细胞因子和氧化应激,导致全身炎症.
结论:
- 斯旺森因因增加肠道透性和随后的LPS转位而诱导全身炎症.
- 肠道透性和自由形式的LPS水平被确定为斯瓦宁素毒性的潜在关键触发因素.
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