目的：探讨血小板因子4（platelet factor 4，PF4）对AD细胞模型中小胶质细胞M1/M2极化的潜在影响 及其可能的分子机制。方法：用Aβ1-42处理BV2小胶质细胞诱导AD细胞模型，予以PF4干预。并进一步通 过Trem2-siRNA转染BV2细胞敲低Trem2的表达。CCK8法检测细胞活力；ELISA法检测TNF-α、IL-6、IL-1 β水平；双标免疫荧光法和Western blot法检测Trem2、iNOS、Arg1的表达；RT-qPCR检测Trem2、iNOS、Arg1、 TNF-α、IL-10的mRNA水平；流式细胞术检测吞噬功能。结果：与对照组比较，Aβ1-42组细胞M1表型标志物 （iNOS、TNF-α、IL-1β）、IL-6表达水平显著升高，M2表型标志物（Arg1、IL-10）、Trem2表达显著下降；与Aβ1-42 组比较，（Aβ1-42+PF4）组细胞 M1 表型标志物（iNOS、TNF-α、IL-1β）、IL-6 表达降低，M2 表型标志物（Arg1、 IL-10）、Trem2表达升高，细胞对Aβ1-42的吞噬能力增强。但是与（Trem2-siRNA+Aβ1-42）组相比，（Trem2-siRNA+Aβ1-42+PF4）组PF4在BV2细胞中无法发挥上述作用。结论：PF4可通过Trem2调节小胶质细胞极化，减 轻AD相关神经炎症，促进Aβ1-42清除。

To investigate the potential impact of platelet factor 4 (PF4) on the M1/M2 polarization of microglia in an Alzheimer's disease (AD) cell model and its possible molecular mechanisms. Methods: An AD cell model was induced by treating BV2 microglial cells with A β 1-42, followed by PF4 intervention. Furthermore, Trem2 expression was knocked down in BV2 cells through Trem2-siRNA transfection. Cell viability was assessed using the CCK8 assay; levels of TNF-α, IL-6, and IL-1β were measured by ELISA; the expressions of Trem2, iNOS, and Arg1 were detected via double-label immunofluorescence and Western blot analyses; mRNA levels of Trem2, iNOS, Arg1, TNF-α, and IL-10 were determined by RT-qPCR; and phagocytic function was evaluated using flow cytometry. Results: Compared with the control group, the A β 1-42 group exhibited significantly elevated expression levels of M1 phenotype markers (iNOS, TNF-α, IL-1 β) and IL-6, along with markedly decreased expression of M2 phenotype markers (Arg1, IL-10) and Trem2. In contrast, the (A β1-42+PF4) group showed reduced expression of M1 phenotype markers (iNOS, TNF-α, IL-1β) and IL-6, increased expression of M2 phenotype markers (Arg1, IL-10) and Trem2, and enhanced phagocytic capacity for A β 1-42 compared with the Aβ1-42 group. However, compared with the (Trem2-siRNA+Aβ1-42) group, PF4 failed to exert the aforementioned effects in BV2 cells in the (Trem2-siRNA+Aβ1-42+PF4) group. Conclusion: PF4 can regulate microglial polarization via Trem2, alleviate AD-related neuroinflammation, and promote the clearance of Aβ1-42.