G-蛋白结合受体1参与Jurkat细胞中甲基四双A诱导的炎症反应
Xiaoyu Lu1, Mengjie Yu1, Yingxin Yang1
1Institute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China.
Toxics
|July 26, 2024
概括
甲基四双 (TCBPA) 激活了G蛋白结合受体1 (GPER1) 途径,增加了免疫细胞中的炎症标志物. 这项研究澄清了TCBPA.
科学领域:
- 免疫学 免疫学 免疫学
- 内分泌学 在内分泌学.
- 毒理学 毒理学 毒理学
背景情况:
- 雌激素通过雌激素受体α (ERα) 影响免疫反应.
- G蛋白结合受体1 (GPER1) 在雌激素介导免疫调节中的作用尚未完全理解.
- 甲基四双 (TCBPA) 是一种具有雌激素活性的环境化学物质.
研究的目的:
- 为了研究TCPA对Jurkat细胞中免疫炎症指标的影响.
- 阐明GPER1在调解TCPA对炎症的影响中的作用.
主要方法:
- 用不同度的TCBPA处理了jurkat细胞.
- 测量了细胞内活性氧物种 (ROS) 的水平.
- 分析了关键信号分子 (ERα,GPER1,PI3K,Akt) 和炎症性细胞因子 (IL1β,IL2,IL6,IL8,IL12α,TNFα) 的蛋白质和mRNA表达.
- 使用GPER1抑制剂G15来评估途径的参与.
主要成果:
- TCBPA以剂量依赖的方式改变了Jurkat细胞的活力.
- TCBPA增加了细胞内ROS水平,并上调了ERα和GPER1的表达.
- TCBPA激活了PI3K/Akt信号通路,由增加的p-Akt和上调的PI3K/AktmRNA证明.
- TCBPA治疗导致了炎症性细胞因子的表达增加.
- 抑制GPER1减弱的PI3K/Akt通路和炎症基因表达的TCPPA诱导激活.
结论:
- 在Jurkat细胞中,TCPA诱导炎症反应.
- 通过GPER1介导的PI3K/Akt信号通路对于TCPPA的促炎作用至关重要.
- 这项研究揭示了TCPA诱导的炎症的新机制.
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