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双甲酸乙通过p38MAPK/NF-κB/NLRP3介导的烧致使肝纤维化

Siming Huo¹, Bo Li¹, Jiayu Du¹

¹Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.

The Science of the total environment

|July 13, 2023

概括

丁丁甲酸 (DBP) 通过激活NLRP3炎症体和p38MAPK/NF-κB通路,导致肝炎和纤维化,导致肝损伤. 针对这些途径可以防止DBP诱导的肝损伤.

科学领域:

环境毒理学环境毒理学
肝病学肝病学是一种肝病学.
分子生物学分子生物学

背景情况:

双甲酸盐 (DBP) 是一种广泛使用的增塑剂,也是全球新发现的一种有机污染物.
暴露于DBP可以激活NLRP3炎症体,诱导炎症性肝损伤,但其精确的肝毒性机制尚未完全理解.

研究的目的:

为了研究DBP诱导的肝损伤背后的分子通路.
阐明NLRP3炎症体和p38MAPK/NF-κB信号通路在DBP肝毒性中的作用.

主要方法:

在C57BL/6N小鼠中,给予DBP (10和50mg/kgB.W.) 在28天内.
在体外共培养HepG2和LX-2细胞与DBP,然后用p38MAPK,NF-κB和NLRP3抑制剂进行治疗.
分析肝脏原沉积,纤维化标记物,热蛋白和信号通路激活.

主要成果:

在小鼠中,DBP的使用增加了肝脏原沉积和纤维化标志物.
DBP上调调节了p38MAPK/NF-κB信号通路和与热相关的蛋白质.
抑制剂治疗缓解了DBP诱导的LX-2细胞激活,p38MAPK/NF-κB信号传递和热.

结论:

暴露于DBP会通过通过p38MAPK/NF-κB信号通路的肝细胞的NLRP3介导的烧亡诱导肝纤维化.
DBP激活肝脏星状LX-2细胞,导致肝纤维化.
准p38MAPK,NF-κB和NLRP3为DBP诱导的肝纤维化提供了潜在的治疗策略.

关键词:

双乙烯甲酸二甲酸乙 (Dibutyl phthalate) 是一种一种肝脏纤维化肝脏纤维化在 NF-κBB 中.通过NLRP3介导的烧灭症.在p38MAPKK中

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