Effect of cypermethrin on thyroid follicular epithelial cell injury via the ROS-NF-κB-NLRP3 pathway

IF 2.9 3区医学 Q2 TOXICOLOGY

Toxicology letters Pub Date : 2025-05-15 DOI:10.1016/j.toxlet.2025.05.008

Leina Jia , Xiaoning Meng , Yu Ma , Jinyu Luo , Xiaoqi Luo , Huifang Yang , Jian Zhou

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Abstract

Cypermethrin (CYP, IUPAC name: [cyano-(3-phenoxyphenyl)methyl] 3-(2,2-dichloroethenyl)-2,2-dimethylcyclopropane-1-carboxylate), a type II pyrethroid insecticide, is suggested to have potential adverse effects on human endocrine, immune, and neurotoxic systems. Objectives: In this study, we aimed to investigate whether CYP causes oxidative stress and pyroptosis in thyroid follicle epithelial cells through the activation of the ROS-NFκB-NLRP3 pathway, thereby causing inflammatory responses. Methods: Nthy-ori 3–1 cells were used as an in vitro model and exposed to CYP at different doses (0, 100, 200, 400, 800, and 1600 μmol/L) for 24 h. Results: CYP treatment enhanced oxidative damage in Nthy-ori 3–1 cells, characterized by cellular crumpling, indistinct borders, increased cellular gaps, appearance of intercellular grease droplets, and increased pyroptosis. Subsequent treatment with the caspase-1 inhibitor VX-765 enhanced cell viability in the VX-765 +CYP group, improving cell morphology, reducing pyroptotic vesicles, suppressing oxidative stress, and downregulating Interleukin-18(IL-18) (an inflammatory factor) level. Conclusion: The results demonstrate that CYP induces pyroptosis in Nthy-ori 3–1 cells through activation of the reactive oxygen species (ROS)-NF-κB-NLRP3 pathway.

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氯氰菊酯通过ROS-NF-κB-NLRP3通路对甲状腺滤泡上皮细胞损伤的影响

氯氰菊酯(CYP， IUPAC名称：[氰-（3-phenoxyphenyl)methyl] 3-（2,2-二氯乙烯基）-2,2-二甲基环丙烷-1-羧酸酯）是一种II型拟除虫菊酯杀虫剂，被认为对人体内分泌、免疫和神经系统有潜在的不良影响。目的：本研究旨在探讨CYP是否通过激活ROS-NFκB-NLRP3通路引起甲状腺滤泡上皮细胞氧化应激和焦亡，从而引起炎症反应。方法：以Nthy-ori 3-1细胞为体外模型，分别以不同剂量（0、100、200、400、800、1600 μmol/L）暴露于CYP 24 h。结果：CYP增强Nthy-ori 3-1细胞的氧化损伤，表现为细胞皱缩、边界模糊、细胞间隙增加、细胞间出现脂滴、焦亡增加。随后用caspase-1抑制剂VX-765治疗VX-765 +CYP组，增强细胞活力，改善细胞形态，减少焦性囊泡，抑制氧化应激，下调白细胞介素-18(IL-18)（一种炎症因子）水平。结论：CYP通过激活活性氧（reactive oxygen species， ROS）-NF-κB-NLRP3通路诱导Nthy-ori 3-1细胞焦亡。

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