The toxicity of synthetic pyrethroids has garnered attention, and studies have revealed that pyrethroids promote fat accumulation and lead to obesity in mice. Nevertheless, the effect of β-cypermethrin (β-CYP) on adipogenesis and its underlying mechanism remains largely unknown. In this study, mouse embryo fibroblasts 3T3-L1 cells were exposed to β-CYP, and the cell viability, intracellular reactive oxygen species (ROS) level, autophagy, and adipogenesis were assessed to investigate the roles of oxidative stress and autophagy in the toxic effects of β-CYP on adipogenesis. The results demonstrated that treatment with 100 μΜ β-CYP elevated the ROS level, decreased mitochondrion membrane potential, stimulated autophagy, and enhanced the adipogenesis induced by the mixture of insulin, dexamethasone, and 3-isobutyl-1-methylxanthine. However, co-treatment with N-acetyl-L-cysteine partially blocked the abovementioned effects of β-CYP in 3T3-L1 cells. In addition, co-treatment with rapamycin, an autophagy agonist, enhanced the inductive effect of β-CYP on adipogenesis, whereas co-treatment with 3-methyladenine blocked the enhancement of adipogenesis caused by β-CYP. Moreover, β-CYP also altered the microenvironment of 3T3-L1 cells to an adipogenesis-friendly one by reducing the extracellular expression of miR-34a, suggesting that the culture media of β-CYP-treated 3T3-L1 cells could shift macrophages to M2 type. Taken together, the data obtained in the present study demonstrated that β-CYP promoted adipogenesis via oxidative stress-mediated autophagy disturbance, and it caused macrophage M2 polarization via the alteration of miR-34a level in the microenvironment. The study demonstrated the adipogenesis-promoting effect of β-CYP and unveiled the potential mechanism.

中文翻译：

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β-氯氰菊酯通过诱导自噬和塑造对脂肪形成友好的微环境来促进3T3-L1细胞的脂肪形成。

合成拟除虫菊酯的毒性已引起人们的关注，研究表明，拟除虫菊酯可促进脂肪积累并导致小鼠肥胖。然而，β-氯氰菊酯（β-CYP）对脂肪形成的作用及其潜在机制仍然未知。在这项研究中，小鼠胚胎成纤维细胞3T3-L1细胞暴露于β-CYP，并评估了细胞活力，细胞内活性氧（ROS）水平，自噬和成脂作用，以研究氧化应激和自噬在毒性中的作用。 β-CYP对脂肪形成的影响。结果表明，用100μMβ-CYP治疗提高了ROS水平，降低了线粒体膜电位，刺激了自噬，并增强了由胰岛素，地塞米松和3-异丁基-1-甲基黄嘌呤的混合物诱导的脂肪形成。然而，ñ-乙酰基-L-半胱氨酸部分阻断了3T3-L1细胞中β-CYP的上述作用。此外，与雷帕霉素（一种自噬激动剂）共同处理可增强β-CYP对脂肪形成的诱导作用，而与3-甲基腺嘌呤共同处理可阻止由β-CYP引起的脂肪形成的增强。此外，β-CYP还可以通过降低miR-34a的细胞外表达，将3T3-L1细胞的微环境改变为成脂友好的细胞，这表明经β-CYP处理的3T3-L1细胞的培养基可以将巨噬细胞转移至M2。类型。综上所述，本研究获得的数据表明，β-CYP通过氧化应激介导的自噬紊乱促进脂肪生成，并通过微环境中miR-34a水平的改变引起巨噬细胞M2极化。