CAJ | 학술논문

目的观察胰腺癌细胞株对神经细胞轴突延伸的促进作用,并分析其可能的机制.方法用倒置显微镜成像系统动态观察胰腺癌细胞与脊髓背根神经节细胞共培养后后者活力,胞体大小及轴突长度与单独培养差异;尼氏染色观察神经细胞活力状态;神经丝蛋白(NF)免疫细胞化学染色观察轴突延伸情况,ELISA检测细胞培养上清液中胰岛素样生长因子-1(IGF-1)含量,并对结果进行统计学分析.结果与单独培养脊髓背根神经节细胞(DRGn)比较,共培养组细胞胞体大小和轴突生长状况优于前者(P＜0.05);神经元活力状态优于前者;NF免疫细胞化学染色结果与倒置显微镜显示结果一致;上清液中IGF-1含量较未培养培养基及空白组较高,差异有统计学意义.结论胰腺癌细胞株与脊髓背根神经节细胞共培养可提高神经元的存活能力,促进轴突延伸,其作用可能是通过癌细胞分泌的细胞因子起作用.
목적 관찰이선암세포주대신경세포축돌연신적촉진작용,병분석기가능적궤제.방법 용도치현미경성상계통동태관찰이선암세포여척수배근신경절세포공배양후후자활력,포체대소급축돌장도여단독배양차이;니씨염색관찰신경세포활력상태;신경사단백(NF)면역세포화학염색관찰축돌연신정황,ELISA검측세포배양상청액중이도소양생장인자-1(IGF-1)함량,병대결과진행통계학분석.결과 여단독배양척수배근신경절세포(DRGn)비교,공배양조세포포체대소화축돌생장상황우우전자(P＜0.05);신경원활력상태우우전자;NF면역세포화학염색결과여도치현미경현시결과일치;상청액중IGF-1함량교미배양배양기급공백조교고,차이유통계학의의.결론 이선암세포주여척수배근신경절세포공배양가제고신경원적존활능력,촉진축돌연신,기작용가능시통과암세포분비적세포인자기작용.
Objective To explore the promotion of pancreatic cancer cell line to axon elongation of nerve cell and to analyze its possible mechanism.Methods The mouse dorsal root ganglion neurons (DRGn) were co-cultured with pancreatic cancer cell line-MIA PaCa-2 and DRGn only were cultured as control.The inverted microscope imaging system was used to observe dynamic change of neuron cyton size and axon length;Nissl' s staining was used to observe neuron vital impulse;Neurofilament (NF) immunocytochemical stain was used to observe axon elongation.Enzyme linked immunosorbent assay (ELISA) was used to detect the concentration of insulin-like growth factor-1 ( IGF-1 ) in the supernatant of culture.Statistical analysis was performed to analyze the result.Results The neuron cyton size in model group was 1.14-fold,1.11-fold,1.29-fold and 1.33-fold ; and the axon length was 1.27-fold,1.48-fold,1.93-fold and 2.0g-fold of that in controls at Ist ,4th,Tth,14th day,respectively.The neuron vital impulse in model group was better than in control group and the results of NF immunocytochemical stain was coincident with the result of inverted microscope imaging system with a significant correlation ( P＜0.05 ).Conclusion In the presence of MIA PaCa-2 cell line,the cytan size,axon length and vital impulse of DRGn were promoted,which was possibly related with a group of growth factors secreted in the microenvironment by nerve and/or cancer cells.