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乌斯提洛辛通过TLR2/MAPK/NF-κB通路诱导损伤

Yingchun Du¹, Guomei Zhang¹, Xuming Zhou¹

¹School of Public Health, Hangzhou Medical College, Hangzhou, Zhejiang, 310013, China.

Toxicon : official journal of the International Society on Toxinology

|October 24, 2025

概括

通过激活托尔类受体2 (TLR2) /线素激活蛋白激酶 (MAPK) /核因子-卡帕B (NF-κB) 途径,乌斯蒂洛辛暴露会导致损伤. 这项研究阐明了ustiloxin诱导的功能障碍和纤维化背后的分子机制.

科学领域:

毒理学毒理学毒理学
分子生物学分子生物学
脏生理学脏生理学

背景情况:

乌斯提洛辛与功能异常有关,但损伤的机制尚不清楚.
托尔类受体2 (TLR2) /线原激活蛋白激酶 (MAPK) /核因子-卡帕B (NF-κB) 途径与炎症反应有关.

研究的目的:

调查TLR2/MAPK/NF-κB通路在乌斯蒂洛辛诱导的损伤中的作用.
为了阐明底层的分子机制使用西托洛克辛毒性.

主要方法:

在雄性小鼠中进行的转录组分析和体内实验,这些小鼠在三个月内暴露于乌斯蒂洛辛 (2,5 12.5 mg/kg).
评估功能指标 (BUN,CR,UA),组织病理学 (H&E,马森染色),以及关键通路和纤维化标记的蛋白质/mRNA表达 (西部斑点,qRT-PCR).

主要成果:

乌斯蒂洛辛暴露导致功能受损,BUN,CR和UA水平升高,并导致细胞病理损伤和间歇性纤维化.
观察到酸化p65,p38,ERK和JNK的蛋白质表达增加,表明TLR2/MAPK/NF-κB通路的激活.
乌斯蒂洛辛暴露显著上调了转化生长因子-β (TGF-β) 的mRNA和蛋白质水平,α-平滑肌肉活性蛋白 (α-SMA) 和纤维化的主要标志物维门丁.

结论:

乌斯提洛辛通过激活TLR2/MAPK/NF-κB信号通路,诱导损伤和纤维化.
这些发现突出了ustiloxins作为损伤的潜在风险因素,并为其毒性提供了机制性的见解.

关键词:

纤维化纤维化纤维化造成脏损伤的人.通过MAPK路径.乌斯蒂洛辛是使用的.

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