Studies have elucidated that pyrethroids induce adipogenesis. It is also known that macrophages can affect the homeostasis of adipose tissue. However, whether and how the β‐cypermethrin (β‐CYP)‐mediated inhibition of the macrophages affects adipogenesis remain unknown. To explore the effects of β‐CYP on adipogenesis through modulating the function of macrophages, 3T3‐L1 cells, a preadipocyte cell line, were exposed to culture medium from either RAW 264.7 cells, a macrophage cell line (RM), or β‐CYP‐treated RAW 264.7 cells (CRM). CRM decreased the inhibitory effects of RM treatment on cell proliferation and adipogenesis, as lipid accumulation, the CEBPA content, and Fasn and Acaca expression in 3T3‐L1 cells were higher following CRM treatment than following RM treatment through the higher levels of the demethylated CEBPA promoter in 3T3‐L1 cells. However, the medium from β‐CYP‐ and N‐acetyl‐L‐cysteine‐cotreated RAW 264.7 cells (CNRM) partially restored the inhibitory effects of RAW 264.7 cells on 3T3‐L1 cells that had been reduced by CRM, indicating that β‐CYP might reduce the cytotoxicity and inhibitory effects of RAW 264.7 cells on the adipogenesis of 3T3‐L1 cells through elevating ROS levels in RAW 264.7 cells. Moreover, exposure to β‐CYP downregulated the TNF‐α secretion in RAW 264.7 cells. In conclusion, these data demonstrated that β‐CYP affected the function of RAW 264.7 cells, alleviating their inhibitory effects on adipogenesis and CEBPA demethylation in 3T3‐L1 cells. β‐CYP might achieve these effects through downregulating the secretion of TNF‐α via elevating ROS levels in RAW 264.7 cells. Our experiments provide a new perspective on the obesogenic effect of pyrethroids.

中文翻译：

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β-氯氰菊酯减轻了RAW 264.7细胞培养基对3T3-L1细胞成熟为脂肪细胞的抑制作用。

研究表明拟除虫菊酯可诱导脂肪形成。还已知巨噬细胞可影响脂肪组织的稳态。然而，β-氯氰菊酯（β-CYP）介导的巨噬细胞抑制作用是否以及如何影响成脂作用仍未知。为了通过调节巨噬细胞的功能探索β-CYP对脂肪形成的影响，将3T3-L1细胞（一种前脂肪细胞系）暴露于RAW 264.7细胞，巨噬细胞系（RM）或β-CYP的培养基中RAW 264.7细胞（CRM）。CRM降低对细胞增殖和脂肪生成RM治疗的抑制作用，脂质积累，CEBPA内容，和FASN和ACACACRM处理后3T3-L1细胞中的表达高于RM处理后，因为3T3-L1细胞中较高水平的去甲基CEBPA启动子。但是，β-CYP-和N-乙酰基-L-半胱氨酸共处理的RAW 264.7细胞（CNRM）的培养基部分恢复了RAW 264.7细胞对CRM降低的3T3-L1细胞的抑制作用，表明β- CYP可能通过提高RAW 264.7细胞中的ROS水平来降低RAW 264.7细胞对3T3-L1细胞脂肪形成的细胞毒性和抑制作用。此外，暴露于β-CYP会下调RAW 264.7细胞中TNF-α的分泌。总之，这些数据表明β-CYP影响RAW 264.7细胞的功能，减轻其对脂肪生成和CEBPA的抑制作用3T3-L1细胞中的甲基化。β-CYP可能通过上调RAW 264.7细胞中的ROS水平而下调TNF-α的分泌来实现这些作用。我们的实验为拟除虫菊酯的致肥胖作用提供了新的视角。