论文部分内容阅读
目的:初步探讨髓样细胞触发受体-2(triggering receptors expressed on myeloid cells-2,TREM-2)过表达对小鼠肺成纤维细胞凋亡的影响。方法:将小鼠肺成纤维细胞分成脂多糖(lipopolysaccharide,LPS)组、LPS+转染试剂组、LPS+空质粒组和LPS+TREM-2过表达质粒组。构建TREM-2过表达质粒,瞬时转染小鼠肺成纤维细胞,RT-PCR检测小鼠肺成纤维细胞中TREM-2 mRNA的表达。荧光显微镜下观察细胞的凋亡。结果:转染TREM-2过表达质粒的小鼠肺成纤维细胞高表达TREM-2;LPS诱导后凋亡细胞明显增多,TREM-2过表达质粒组凋亡细胞数少于空质粒转染组和LPS组。结论:TREM-2可抑制LPS诱导的小鼠肺成纤维细胞凋亡,提示TREM-2参与调控肺成纤维细胞的数量,可能与肺组织的生长发育及损伤修复有关。
Objective: To investigate the effect of triggering receptors expressed on myeloid cells-2 (TREM-2) overexpression on the apoptosis of mouse lung fibroblasts. Methods: Mouse lung fibroblasts were divided into lipopolysaccharide (LPS) group, LPS + transfection reagent group, LPS + empty plasmid group and LPS + TREM-2 over-expression plasmid group. TREM-2 overexpression plasmid was constructed and transfected into mouse lung fibroblasts transiently. The expression of TREM-2 mRNA in mouse lung fibroblasts was detected by RT-PCR. Cell apoptosis was observed under a fluorescence microscope. Results: TREM-2 cells were highly expressed in lung fibroblasts transfected with TREM-2 overexpression plasmid; apoptotic cells were significantly increased in LPS-treated cells, but less in TREM-2 overexpression plasmid group than in empty plasmid transfected group And LPS group. CONCLUSION: TREM-2 can inhibit LPS-induced lung fibroblast apoptosis, suggesting that the number of TREM-2 involved in the regulation of lung fibroblasts may be related to the growth and damage of lung tissue repair.