谷氨通过宿主微生物群相互作用和CAR依赖途径,有助于缓解肝损伤
Xuan Xiang1,2,3, Siwei Liu1,2, Houfu Wang2
1Hunan Provincial Key Laboratory of Animal Intestinal Function and Regulation, Hunan International Joint Laboratory of Animal Intestinal Ecology and Health, College of Life Sciences, Hunan Normal University, Changsha, 410081, China.
Science China. Life sciences
|October 12, 2025
概括
外源性谷氨 (GSH) 补充剂通过改善宿主微生物群相互作用和激活构成性安德罗受体 (CAR) 途径来缓解肝损伤. 这种抗氧化剂治疗可以增强小猪的免疫功能和肠道健康.
科学领域:
- 生物化学 生物化学
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
背景情况:
- 谷氨 (GSH) 是一种关键的抗氧化剂,但其在通过宿主微生物群和肝脏相互作用减轻压力诱导的肝损伤方面的作用尚未完全理解.
- 氧化应激和炎症有助于肝损伤,影响整体健康和免疫功能.
研究的目的:
- 调查外源性GSH补充剂在减轻肝损伤中的调节机制.
- 确定宿主微生物群相互作用和构成性安德罗斯坦受体 (CAR) 途径在GSH保护作用中的作用.
主要方法:
- 在体内研究:28天大的猪被食了不同的GSH水平,随后注射了帕拉克瓦特 (PQ) 诱导肝损伤.
- 试验室研究:阿尔法小鼠肝12 (AML12) 细胞暴露于有或没有GSH和CAR抑制剂 (CINPA1) 的三甲基氧化物 (tBHP).
- 分析包括肝脏形态,免疫标志物 (CD4+/CD8+比,IgA,IL-10),肠道微生物群多样性,CAR活性和基因表达.
主要成果:
- 小猪中PQ诱导的肝损伤通过GSH得到改善,以改善免疫功能和减少炎症为证.
- 草甘治疗增加了有益的肠道细菌的多样性和丰富性,促进了宿主微生物群的相互作用.
- 在体外,GSH通过激活CAR通路来保护AML12细胞免受tBHP诱导的氧化应激,该通路被CINPA1.1.阻止.
结论:
- 外源性GSH补充剂有效地减轻小猪的肝损伤.
- 保护机制涉及调节宿主微生物群相互作用,并激活依赖CAR的信号通路.
- GSH具有作为治疗剂的潜力,用于管理与氧化压力相关的肝脏疾病.
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