为了研究Prdx1在巨噬细胞极化中的作用，用脂多糖（LPS）、干扰素γ（IFNγ）或IL-4处理小鼠单核巨噬细胞（RAW264.7）的白血病细胞，诱导1型巨噬细胞（M1）和1型巨噬细胞分别为巨噬细胞（M2）巨噬细胞。 Prdx1 基因敲除细胞（Prdx1-/-）用于该研究。流式细胞仪检测M1/M2巨噬细胞标志物，ELISA试剂盒测定M1/M2细胞因子水平。还评估了诱导型一氧化氮合酶 (iNOS) 活性、精氨酸酶-1 (Arg-1) 活性和氧化损伤。采用Seahorse XFe24细胞外通量分析仪测量细胞外酸化率和耗氧率。使用线粒体膜电位染料（JC-1）荧光探针分析线粒体膜电位，并通过荧光染色检测线粒体超氧化物。此外，还检查了添加线粒体活性氧 (ROS) 清除剂对 RAW264.7 巨噬细胞极化的影响。结果表明，ROS、过氧化氢和 8-羟基-2 脱氧鸟苷 (8-OHDG) 有所增加。观察到细胞毒性和线粒体毒性作用，包括线粒体超氧化物积累、三磷酸腺苷 (ATP) 产生减少、线粒体膜电位降低和线粒体 DNA 拷贝数减少。此外，线粒体内膜转位酶 23 (TIM23) 线粒体蛋白和线粒体应激蛋白热休克蛋白 60 (HSP60) 下调。 RAW264.7细胞中M1巨噬细胞极化的细胞外酸化率（ECAR）增加，而M2巨噬细胞的耗氧率（OCR）降低。这些发现表明，RAW264.7细胞中的Prdx1敲除可以抑制M2巨噬细胞极化，但通过损害线粒体功能和减少氧化磷酸化来促进M1巨噬细胞极化。

In order to investigate the role of Prdx1 in macrophage polarization, mouse leukemia cells of monocyte macrophage (RAW264.7) were treated with lipopolysaccharides (LPS)+ interferon gamma (IFNγ) or IL-4 to induce type 1 macrophage (M1) and type 1 macrophage (M2) macrophages, respectively. The Prdx1 gene knockout cells (Prdx1-/-) were used for the study. Flow cytometry was conducted to detect M1/M2 macrophage markers, and ELISA kits were used to measure M1/M2 cytokine levels. Inducible nitric-oxide synthase (iNOS) activity, arginase-1 (Arg-1) activity, and oxidative damage were also assessed. The Seahorse XFe24 Extracellular Flux Analyzer was employed to measure extracellular acidification rate and oxygen consumption rate. The mitochondrial membrane potential was analyzed using the mitochondrial membrane potential dye (JC-1) fluorescent probe, and mitochondrial superoxide was detected through fluorescence staining. Additionally, the impact of adding a mitochondrial reactive oxygen species (ROS) scavenger on RAW264.7 macrophage polarization was examined. The results demonstrated an increase in ROS, hydrogen peroxide, and 8-hydroxy-2 deoxyguanosine (8-OHDG). Cytotoxicity and mitochondrial toxic effects, including mitochondrial superoxide accumulation, decreased adenosine-triphosphate (ATP) production, reduced mitochondrial membrane potential, and decreased mitochondrial DNA copy number, were observed. Furthermore, down-regulation of translocase of inner mitochondrial membrane 23 (TIM23) mitochondrial protein and mitochondrial stress protein heat shock protein 60 (HSP60) was noted. The extra cellular acidification rate (ECAR) in M1 macrophage polarization in RAW264.7 cells was increased, while oxygen consumption rate (OCR) in M2 macrophages was reduced. These findings indicate that Prdx1 knockout in RAW264.7 cells can inhibit M2 macrophage polarization but promote M1 macrophage polarization by impairing mitochondrial function and reducing oxidative phosphorylation.