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通过JAK-STAT信号传递的白血病抑制因子驱动16HBE细胞中的酸诱导的上皮-半细胞过渡
Yaqi Li1, Zhanbing Sun2, Yuqi Tong1
1Department of Preventive Medicine, School of Public Health, Hengyang Medical School, University of South China, Hengyang, China.
Journal of applied toxicology : JAT
|May 1, 2025
概括
暴露于硫酸会通过激活JAK-STAT通路并诱导肺细胞上皮-介质细胞过渡 (EMT) 来触发慢性肺病. 通过尼克洛萨米德或LIF静音抑制抑制这种途径,可以降低的毒性.
科学领域:
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 烯化合物具有致癌性,并导致慢性烯疾病.
- 简氏酶信号转换器和转录激活器 (JAK-STAT) 途径对疾病进展至关重要.
- 白血病抑制因子 (LIF) 调节炎症和上皮层-介质细胞过渡 (EMT).
研究的目的:
- 研究JAK-STAT和LIF在人类支气管上皮细胞 (16HBE) 中硫酸盐 (BeSO4) 诱导的EMT中的作用.
- 阐明毒性的分子机制.
主要方法:
- 暴露于16HBE细胞中的BeSO4.4.
- 使用药理抑制 (尼克洛萨米德) 和LIF的基因沉默来准JAK-STAT通路.
- 评估了细胞增殖,形态,炎症和EMT标志物.
主要成果:
- BeSO4抑制了16HBE细胞的增殖,并激活了JAK-STAT通路.
- 尼克洛萨米德减少了BeSO4诱导的炎症和EMT.
- LIF静音降低了JAK-STAT激活和EMT标志物表达.
结论:
- 在16HBE细胞中BeSO4诱导的EMT涉及JAK-STAT通路和LIF的激活.
- 针对JAK-STAT通路可以减轻的毒性.
- 提供了对化合物毒性机制的见解.
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