肿瘤相关巨噬细胞（TAM）向M2表型极化是恶性胸腔积液(MPE)形成的重要机制,其中AMPK介导的TAM自噬是促进其向M2表型极化的关键信号通路。前期临床和实验研究显示：消水方具有抑制肺癌MPE的作用，但在抑制胸膜转移瘤体增殖方面作用较弱，提示消水方减少MPE还可能存在其他机制，而预实验表明消水方可以减少小鼠MPE中M2型TAM的表达。基于此我们提出消水方可能是通过干预AMPK介导的巨噬细胞自噬，调控其表型和功能，进而抑制MPE的产生。本课题拟在此基础上，建立C57BL/6小鼠Lewis肺癌胸腔积液模型和巨噬细胞自噬促表型极化模型，采用透射电镜、流式细胞术、Western blot、RT-PCR等技术，从体内和体外两方面观察消水方对MPE中AMPK介导的TAM自噬及表型极化的影响，进一步揭示消水方治疗MPE的相关机制，为MPE的临床治疗提供新思路。

Inhibiting the polarization of M2 phenotype tumor-associated macrophage (TAM) is an important therapeutic mechanism for malignant pleural effusion (MPE), and macrophage autophagy induced by AMPK could regulate the polarization of macrophage. Xiaoshui decoction could reduce MPE which have been demonstrated by our previous clinical and experimental studies, but there is little inhibition effect of Xiaoshui decoction on tumor proliferation, indicating that some other mechanism exists. The pre-expriment showed that Xiaoshui Decoction could decrease the expression of M2 phenotype macrophages in MPE of mice. So we presume that Xiaoshui decoction could reduce MPE by regulating autophagy to control the polarization and function of macrophage. By establishing C57BL/6 mice lung cancer MPE model and macrophage phenotypic polarization model induced by autophagy, we will employ methods including transmission electron microscope, flow cytometry, western blot, RT-PCR et al to evaluate the effect of Xiaoshui decoction on AMPK-induced autophagy and polarization of macrophages in vivo and in vitro. This study will reveal new mechanism of Xiaoshui decoction treating MPE and provide the novel method for MPE.