迪索代基基酸通过对抗肝 X 受体α 的作用促进泡细胞的形成
Xinming Shen1, Qiang Li2, Chong Huang2
1MOE Laboratory for Earth Surface Processes, College of Urban and Environmental Sciences, Peking University, Beijing 100871, China; School of Public Health, Zhengzhou University, Zhengzhou 450001, China.
Journal of hazardous materials
|July 4, 2024
概括
二基基酸盐 (DIDPP) 是一种常见的环境污染物,可能会促进动脉样硬化. 这项研究揭示了DIDPP对抗肝X受体α (LXRα),破坏巨细胞中的胆固醇调节并增加泡细胞的形成.
科学领域:
- 环境科学 环境科学
- 毒理学 毒理学 毒理学
- 心血管生物学 心血管生物学
背景情况:
- 有机阻燃剂 (OPFR) 是已知的心血管毒素.
- 双基基酸盐 (DIDPP) 广泛使用,并在环境中检测到.
- DIDPP在动脉样硬化发展中的作用尚不清楚.
研究的目的:
- 调查DIDPP诱导动脉样硬化的潜力.
- 探索DIDPP和肝脏X受体 (LXRs) 之间的相互作用,这是动脉样硬化的主要调节者.
- 阐明DIDPP对胆固醇代谢的影响背后的分子机制.
主要方法:
- 在体外巨模型.
- 在不同度 (1-10μM) 的DIDPP治疗.
- 对LXRα目标基因表达的分析 (ABCA1,ABCG1,SR-B1).
- 测量胆固醇外流和泡细胞的形成.
- 对胆固醇流入的评估.
主要成果:
- DIDPP作为一个LXRα对抗剂 (IC50 = 16.2μM).
- DIDPP降低了LXRα基因的下调,降低了胆固醇排放量7.9-13.2%.
- DIDPP治疗以剂量依赖的方式增加了24.1-43.1%的泡细胞形成.
- DIDPP不会影响胆固醇的流入,这表明一种与流出相关的机制.
结论:
- DIDPP表现出LXRα对抗性的活性.
- DIDPP通过破坏巨细胞中的胆固醇外流来促进动脉样硬化.
- 对DIDPP的环境暴露可能构成动脉样硬化发展的风险.
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