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香烟烟雾引起的前列腺素输送物SLCO2A1表达的衰减,通过阿里碳化合物受体表达

Melody N Shumba¹, Yoshinobu Nakamura¹, Takeo Nakanishi¹

¹Laboratory of Membrane Transport and Biopharmaceutics, Faculty of Pharmacy, Takasaki University of Health and Welfare, Takasaki, 370-0033, Japan.

Prostaglandins & other lipid mediators

|November 28, 2024

概括

香烟烟雾提取物 (CSE) 通过激活基碳水化合物受体 (AHR) 来降低炎症敏感细胞中的SLCO2A1表达. 这项研究揭示了一种毒理机制,通过前列腺素载体调节将烟草烟雾与炎症联系起来.

科学领域:

毒理学毒理学毒理学
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

前列腺素载体SLCO2A1调节前列腺素E2 (PGE2),这是一个炎症媒介.
以前的研究表明,香烟烟雾提取物 (CSE) 在老鼠肺细胞中降低Slco2a1mRNA.
受烟草吸烟引起的炎症影响的器官包括肺和结肠.

研究的目的:

为了研究CSE对人类SLCO2A1mRNA在相关细胞系中的表达的影响.
阐明CSE对SLCO2A1转录的影响背后的分子机制.

主要方法:

将SLCO2A1 5'-边缘区域分克隆为一个光酶报告载体.
报告员测试用于评估CSE暴露后的促进者活动.
在各种人类细胞系 (结肠,肺,肝脏) 中分析SLCO2A1mRNA和蛋白质表达.
评估使用抗剂和配体的烯碳化合物受体 (AHR) 的作用.

主要成果:

CSE显著降低了结肠 (LoVo,Caco-2) 和肺 (NCI-H292) 细胞中的SLCO2A1mRNA和促进体活性,但没有降低肝脏 (HepG2) 细胞的活性.
长期的CSE暴露消除了LoVo细胞中的SLCO2A1蛋白表达.
CSE对SLCO2A1的抑制作用与AHR激活有关,这是通过AHR抗剂 (PD98059) 的恢复和AHR配体 (β-纳夫托夫拉) 的减少所证明的.
突变异种生物反应元件取消了CSE的负面监管效应.
抑制AHR减少了CSE对SLCO2A1mRNA表达的负面影响.

结论:

在人类结肠和肺细胞中,CSE通过AHR激活来负调节SLCO2A1转录.
这种机制提供了对烟草烟雾如何导致炎症的毒理学见解.
准AHR信号可能是缓解烟雾引起的炎症的策略.

关键词:

亚利碳化合物受体 (AHR) 是一种香烟烟雾 (CS) 是指香烟的烟雾.前列腺腺素载体运输体这就是SLCO2A1的原因.异生生物反应元素 (XRE)

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