CAJ | 학술논문

为了探讨细胞外基质（extracellular matrix，ECM）对体外培养的小鼠子宫内膜细胞生长形态以及抗原递呈作用中 MHCⅡ表达的影响，对小鼠子宫内膜细胞进行分离鉴定，分别在添加了 ECM 的细胞培养板上和未添加 ECM 的细胞培养板同时对小鼠子宫内膜上皮细胞和基质细胞进行培养，观察生长形态，并采用免疫组化法，分别检测1、3、5 d MHCⅡ表达水平，进行图像分析比较。结果表明，生长形态有明显差异，且添加 ECM的细胞培养板上2种细胞生长速度明显比未添加 ECM 的培养板上的细胞生长速度慢；免疫组化结果，未添加ECM 培养板中上皮细胞和基质细胞在1、3 d MHCⅡ表达均为阳性，且表达水平都逐渐降低，在第5天时，2种细胞 MHCⅡ表达均为阴性，而添加了 ECM 的细胞培养板上2种细胞由于生长速度缓慢，第5天 MHCⅡ仍有表达。因此，在 ECM 的参与下，体外培养的小鼠子宫内膜细胞的生长形态发生了改变、生长速度有所延缓，同时延长了 MHCⅡ的表达。。
위료탐토세포외기질（extracellular matrix，ECM）대체외배양적소서자궁내막세포생장형태이급항원체정작용중 MHCⅡ표체적영향，대소서자궁내막세포진행분리감정，분별재첨가료 ECM 적세포배양판상화미첨가 ECM 적세포배양판동시대소서자궁내막상피세포화기질세포진행배양，관찰생장형태，병채용면역조화법，분별검측1、3、5 d MHCⅡ표체수평，진행도상분석비교。결과표명，생장형태유명현차이，차첨가 ECM적세포배양판상2충세포생장속도명현비미첨가 ECM 적배양판상적세포생장속도만；면역조화결과，미첨가ECM 배양판중상피세포화기질세포재1、3 d MHCⅡ표체균위양성，차표체수평도축점강저，재제5천시，2충세포 MHCⅡ표체균위음성，이첨가료 ECM 적세포배양판상2충세포유우생장속도완만，제5천 MHCⅡ잉유표체。인차，재 ECM 적삼여하，체외배양적소서자궁내막세포적생장형태발생료개변、생장속도유소연완，동시연장료 MHCⅡ적표체。。
In order to investigate the effects of ECM on the morphology and expression of MHCⅡof mouse endometrial cells cultured in vitro ,the mouse endometrial cells were isolated and identified.The morphol-ogy of the cells cultured in vitro containing the ECM or no ECM were observed respectively,and the MHCⅡ expression level of the cells on 1,3,5 days were detected by immunohistochemistry and image analysis methods.The results showed that:The growth morphology of the cells cultured containing the ECM or no ECM had significant difference,and the growth rate of the cells cultured containing the ECM were slower than the growth rate of the cells cultured no ECM.The expression of MHCⅡ in epithelial cells and the stromal cells cultured no ECM were positive,and the expression levels were gradually reduced,and on the fifth day,the expression of MHCⅡwere negative in two kinds of cells.But,the expression of MHCⅡ in epithelial cells and the stromal cells cultured containing ECM were positive on the fifth day.Therefore, under the guidance of ECM,the growth morphology of mouse endometrial cells cultured in vitro changed, the growth rate slowed,and at the same time,the expression of MHCⅡ prolonged.