在肝中,GPR120通过调解由乙醇诱导的巨细胞M1极化来加剧免疫炎症反应
Yue Zhang1, Hongmin Lu1, Lulu Hou1
1College of Wildlife and Protected Area, Northeast Forestry University, Harbin, Heilongjiang 150040, PR China.
Journal of hazardous materials
|December 22, 2024
概括
酸除草剂通过诱导炎症和细胞死亡来损害肝. 用Omega-3作为GPR120激动剂的补充剂,在动物模型中有效地逆转了这些毒性作用.
科学领域:
- 环境毒理学环境毒理学
- 鸟类病理学 鸟类病理学
- 分子生物学分子生物学
背景情况:
- 乙化是一种普遍存在的除草剂,具有潜在的生态和健康风险.
- 它在中肝脏毒性的特定机制尚不清楚.
- 了解这些影响对于生物安全和鸟类健康至关重要.
研究的目的:
- 为了阐明中乙醇诱导的肝毒性的分子机制.
- 调查GPR120通路在乙烯酸毒性中的作用.
- 探索使用营养补充剂的潜在治疗干预措施.
主要方法:
- 利用动物-细胞-动物模型研究酸盐的作用.
- 进行了转录基因分析,以确定受影响的途径.
- 在细胞系 (LMH,HD11) 中对GPR120进行了基因沉默和激进性实验.
- 在动物研究中使用的欧米茄-3 (GPR120激动剂).
主要成果:
- 暴露于酸盐会导致肝细胞胀,炎症,脂质沉积和编程细胞死亡 (PANoptosis).
- 确定了GPR120通路作为一个关键的调解器,其沉默会加剧损伤和激进减轻效应.
- 欧米茄-3补充剂有效地逆转了酸盐诱导的肝炎和中的PANoptosis.
结论:
- 酸通过涉及GPR120和炎症酶激活的机制诱导的肝损伤和PANoptosis.
- 用Omega-3等激动剂向GPR120通路显示有望减轻除草剂毒性.
- 加强残留物控制和风险评估对于管理酸盐对生态和健康的影响至关重要.
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