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在HepG2细胞中T-2毒素诱导的肝毒性涉及炎症和Nrf2/HO-1通路

Mercedes Taroncher^1,2, Felipe Franco-Campos^1,2, Yelko Rodríguez-Carrasco^1,2

¹Research Group in Alternative Methods for Determining Toxics Effects and Risk Assessment of Contaminants and Mixtures (RiskTox), University of Valencia, 46100 Valencia, Spain.

|August 27, 2025

概括

在谷物中发现的T-2毒素暴露会导致肝细胞的形状变化和炎症. 它还影响氧化应激路径,突出T-2毒素

科学领域:

毒理学
细胞生物学
分子生物学

背景情况:

T-2毒素是一种常见于谷物和谷物食品中的高度有毒的真菌毒素.
通过饮食接触T-2毒素对一般人群构成风险.
了解T-2毒素的细胞机制对于评估其对健康的影响至关重要.

研究的目的:

研究T-2毒素对HepG2细胞的影响,重点关注形态变化,氧化应激和炎症反应.
在暴露于T-2毒素时分析关键的炎症性细胞因子 (IL-1β,IL-6,TNF-α) 和参与氧化应激的蛋白质 (Nrf2,HO-1).

主要方法:

暴露于不同度的T-2毒素 (7. 5, 15 和 30 nM).
使用间接免疫光检测评估了形态变化.
通过 qPCR 和 Western blot 试验量化了mRNA和蛋白质表达水平.

主要成果:

暴露于T-2毒素导致HepG2细胞的度依赖性形态变化,从圆形转变为延长形状.
观察到炎症性细胞因子mRNA (IL- 1β,IL- 6,TNF- α) 的上调,TNF- α在30 nM T-2时显示出最显著的增加.
在所有测试度中,Nrf2/HO-1氧化应激通路被调节,HO-1在低T-2度上升调节,Nrf2降低调节.

结论:

暴露于T-2毒素导致HepG2细胞显著的炎症反应和形态变化.
这项研究证实T-2毒素的肝毒性涉及Nrf2/HO-1通路的调节.
未来的研究应该探索天然抗氧化剂对T-2毒素诱导的损伤的潜在细胞保护作用.

关键词:

T-2 毒素西部污染免疫光发生炎症氧化情况在QPCR中

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