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氧化应激和Keap1-Nrf2通路参与大鼠双A诱导的肝损伤

Juan Tang^1,2, Kai Wang¹, Dan Shen¹

¹College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China.

|January 8, 2025

概括

双甲 (BPA) 暴露会通过诱导氧化应激引起大鼠的肝脏和脏损伤. Keap1-Nrf2通路的激活可能会防止BPA诱导的肝毒性,这表明对人类肝脏疾病的影响.

科学领域:

毒理学毒理学毒理学
分子生物学分子生物学
环境健康环境健康

背景情况:

双A (BPA) 是一种广泛存在的环境污染物,用于塑料和树脂中.
暴露于BPA与肝脏病变有关,但机制尚不清楚.
Keap1-Nrf2信号通路对于细胞防御氧化应激至关重要.

研究的目的:

在大鼠模型中研究Keap1-Nrf2通路在双A诱导的肝毒性中的作用.
阐明BPA诱导的肝损伤背后的分子机制.

主要方法:

鼠被口服BPA (0.5,5,50毫克/公斤) 或玉米油30天.
对肝脏和脏组织进行了组织学,氧化应激和基因/蛋白质表达分析 (qRT-PCR,西式涂抹,免疫组织化学).
评估的关键标志物包括Nrf2,Keap1,氧化应激指标 (MDA,SOD,GPx) 和亡标志物 (caspase-3).

主要成果:

暴露于BPA降低了肝脏和上腺系数,并导致肝脏和脏组织的组织形态损伤.
在接受BPA治疗的老鼠中观察到血清GOT和TNF-α的升高,氧化应激标志物的增加 (MDA,降低SOD/GPx),以及Nrf2,Keap1,GPX2,HO-1和caspase-3的增强表达.
在暴露于BPA的肝脏组织中检测到增加的Nrf2和裂开的caspase-3蛋白水平.

结论:

双甲暴露会诱导肝毒性和脏损伤,与氧化应激和亡有关.
Keap1-Nrf2通路被BPA暴露激活,可能会对肝毒性产生保护作用.
这些发现表明BPA对肝功能构成风险,并突出了调节Keap1-Nrf2通路的治疗潜力,用于管理BPA诱导的肝损伤.

关键词:

这就是HO-1的HO-1.Nrf2 没有任何问题.双 A 是一种双 A.肝毒性肝毒性肝毒性鼠标鼠标鼠标鼠标鼠标

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