解读NLRP3在BPA中介毒性的分子机制:对向疗法的影响
Doveit Antony Charles1, Sabina Evan Prince1
1Department of Biotechnology, School of Biosciences and Technology, VIT, Vellore, Tamil Nadu, India.
Heliyon
|April 10, 2024
概括
双甲 (BPA) 暴露会引发氧化应激,并激活NLRP3炎症酶,导致器官损伤. 准NLRP3可能提供一种治疗策略来对抗BPA诱导的毒性.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 免疫学 免疫学 免疫学
背景情况:
- 双甲 (BPA) 是一种广泛存在于消费品中的工业化学物质.
- 暴露于BPA与免疫和内分泌干扰以及基因毒性有关.
- 类似NOD的受体蛋白3 (NLRP3) 炎症体在炎症过程中至关重要.
研究的目的:
- 审查BPA暴露和NLRP3炎症酶激活之间的关系.
- 探索链接BPA,氧化应激和NLRP3信号的分子机制.
- 讨论BPA诱导的器官毒性和针对NLRP3.3的潜在治疗策略.
主要方法:
- 文献综述侧重于BPA毒理学和NLRP3炎症途径.
- 在BPA诱导的激活中分析信号级联 (PI3K/AKT,JAK/STAT,AMPK/mTOR,ERK/MAPK).
- 研究器官特异性毒性和免疫病原发生.
主要成果:
- BPA诱导氧化应激,导致细胞内自由基的产生.
- 激活的NLRP3炎症酶信号与BPA的不良影响有关.
- 暴露于BPA与肝脏,脏,胃肠道和心血管功能障碍有关.
结论:
- 暴露于BPA会通过氧化应激和特定的信号通路激活NLRP3炎症体.
- NLRP3炎症酶激活有助于由BPA引起的各种器官毒性.
- 准NLRP3炎症酶组为缓解BPA引起的器官损伤提供了潜在的治疗途径.
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