中文摘要：

目的：研究胃癌细胞对巨噬细胞的诱导作用，分析活化巨噬细胞对间皮细胞的损伤作用及机制。方法：人正常胃腺上皮细胞系GES-1 及人低分化胃癌细胞系SGC-7901与人单核巨噬细胞THP-1 共培养，诱导后者分化，研究后者对人腹膜间皮细胞HMR-sv5 的损伤作用及分子机制。结果：胃癌细胞诱导THP-1 形成肿瘤相关巨噬细胞（TAM），M1 型巨噬细胞表面抗原的表达显著下调，而M2 表型的表面抗原明显上调，细胞形态也发生明显改变。TAM显著抑制正常间皮细胞生长，促进间皮细胞凋亡和上皮间质转化。结论：胃癌细胞诱导巨噬细胞发生表型和功能转化，进而导致间皮细胞发生EMT 和凋亡，促进形成腹膜转移癌。

英文摘要：

Objective：This work aims to determine the effects of the induction of gastric cancer cells on macrophages and the damaging effect of activated peritoneal macrophages on the peritoneal mesothelial cells. Methods：The human macrophage cell line THP- 1 was co-cultured with either the human normal gastric epithelial cell line GES-1 or the poorly differentiated human gastric cancer cell line SGC-7901 . The induction effects of the gastric cells on the THP- 1 cells was then studied. The effects of the activated macrophages on the human peritoneal mesothelial cell line HMR-SV 5 were further studied.Results：The gastric cancer cell line SGC-7901 induced THP- 1 cells to become tumor-associated macrophages （TAM）, which had distinctive morphological features. Induction significantly reduced the expression of the M1-type macrophage surface antigens, such as CD80 and CD86 , and significantly increased the expression of the M2-type macrophage surface antigens, such as CD163. The activated macrophages brought about a significant growth inhibition and apoptosis of the mesothelial cell HMR-SV 5, The HMR-SV5 cell also underwent a conspicuous epithelial-mesenchymal transition （EMT）. Conclusion：Gastric cancer cells could induce morphological and phenotypic changes in the macrophages, which can in turn cause mesothelial cell damage, apoptosis, and EMT, thus creating a favorable microenvironment for peritoneal carcinomatosis.