酸通过减弱NF-κB信号通路来减轻二氧化诱导的急性肝毒性
Semiha Orhan1, Ruhi Turkmen2, Hasan Huseyin Demirel3
1Intensive Care Unit Afyonkarahisar, Afyonkarahisar Health Sciences University, Afyonkarahisar, Turkey.
Molecular biology reports
|July 13, 2024
概括
酸 (CGA) 在大鼠中表现出对六价 (二酸,PDC) 诱导的肝脏和脏毒性的保护作用. 在CGA中,CGA就是CGA.
科学领域:
- 毒理学 毒理学 毒理学
- 药理学 药理学是指药理学的学科.
- 生物化学 生物化学
背景情况:
- 六价 (CrVI) 是一种有毒物质,会引起氧化应激和炎症,导致肝毒性和毒性.
- 二酸盐 (PDC) 是 CrVI 暴露的常见来源.
- 酸 (CGA) 具有已知的抗氧化和抗炎性质.
研究的目的:
- 在大鼠模型中研究CGA对PDC诱导的急性肝毒性和毒性的保护作用.
- 评估与PDC暴露和CGA治疗相关的生化,本病学和免疫组织化学变化.
主要方法:
- 威斯塔尔白性大鼠通过腹膜内注射PDC (15 mg/kg) 和CGA (10,20,40 mg/kg) 的不同剂量.
- 生物化学测定测量了血清和组织中的谷氨 (GSH),催化酶 (CAT),介质素-6 (IL-6) 和瘤亡因子-α (TNF-α) 的水平.
- 组织病理学和免疫组织化学分析检查了肝脏和脏组织损伤.
主要成果:
- 暴露于PDC显著增加IL-6并降低了GSH,CAT,TNF-α和IL-1β水平.
- 在肝脏和脏组织中,PDC诱导了可观察到的组织病理学和免疫组织化学损伤.
- 服用CGA,尤其是10mg/kg,可以逆转这些毒性作用,恢复生化标志物和组织完整性.
结论:
- CGA表现出显著的抗氧化和抗炎作用.
- 在老鼠中,CGA有效地减轻PDC暴露引起的急性肝毒性和毒性.
- CGA代表了一种潜在的治疗剂,可以减轻引起的器官损伤.
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