中文摘要：

目的探讨巨噬细胞（THP-1）活化的人脐带间充质干细胞（huc-MSC）对胃癌细胞系HGC-27中血小板源性生长因子（PDGFD）的调控作用。方法将THP-1与huc-MSC直接共培养,观察共培养前后细胞的形态变化;western blot检测huc-MSC中肿瘤相关成纤维细胞（CAF）相关指标;将HGC-27分为阴性对照组、huc-MSC间接共培养组及THP-1活化的huc-MSC间接共培养组,ELISA法检测各组上清液中PDGFD含量;免疫荧光法检测HGC-27中PDGFD的表达;western blot检测HGC-27中JAK1-STAT3通路活化情况。结果与huc-MSC直接共培养后THP-1细胞部分呈纤长形。huc-MSC中E-cadherin蛋白表达下调（P〈0.01）,N-cadherin（P〈0.01）和vimentin（P〈0.01）表达上调,呈现CAF样活化。与阴性对照组比较,huc-MSC和THP-1活化后huc-MSC均促进HGC-27中PDGFD的表达,THP-1活化的huc-MSC较huc-MSC促进作用更显著（P〈0.01）。与阴性对照组比较,huc-MSC和THP-1活化后huc-MSC处理组HGC-27中JAK1和STAT3蛋白水平均显著增加（P〈0.01）,THP-1活化后huc-MSC组较huc-MSC组增加更显著（P〈0.01）。结论 THP-1促进huc-MSC呈CAF样活化,可上调胃癌细胞HGC-27中PDGFD的表达,可能与JAK-STAT3通路活化有关。

英文摘要：

Objective To investigate the regulation of human umbilical cord mesenchymal stem cells（huc-MSC） activated by macrophage（THP-1） on the expression of platelet-derived growth factor D（ PDGFD） in gastric cancer cell line HGC-27. Methods The morphology of huc-MSC before and after co-cultured with THP-1 were observed. The markers related to carcinoma-associated fibroblasts（CAF） in huc-MSC were detected by western blot. The PDGFD levels in the supernatants of HGC-27 cells（negative control）,HCG-27 cells co-cultured with huc-MSC,and HCG-27 cells co-cultured with huc-MSC activated by THP-1 cells were determined by an ELISA method. The expression of PDGFD and the activation status of JAK1-STAT3 pathway in HGC-27 cells were detected by immunofluorescent staining and western blot,respectively. Results After co-cultured with huc-MSC,a few of THP-1 cells appeared fiber-like extensions,and huc-MSC exhibited CAFs-like activation. Meanwhile,the expression of E-cadherin protein in huc-MSC was downregulated（P〈0. 01）,while the expressions of N-cadherin and Vimentin upregulated（ P〈0. 01）. Compared with the negative control,both huc-MSC and THP-1 activated huc-MSC promoted the expression of PDGFD in HGC-27,and the promotion effect of the latter was more obvious than that of the former（P〈0. 01）. Compared with the negative control,the levels of JAK1 and STAT3 in HGC-27 cells treated with huc-MSC or THP-1 activated huc-MSC increased significantly（P〈0. 01）,and the latter increased more than the former（P〈0.01）. Conclusion THP-1 may activate huc-MSC as CAF,which may upregulate the expression of PDGFD in HGC-27 by the activation of JAK1-STAT3 pathway.