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该研究探讨了基质细胞衍生因子-1(stromal cell-derived factor-1,SDF-1)/趋化性细胞因子受体4(chemotaxis cytokine receptor 4,CXCR4)和SDF-1/趋化性细胞因子受体7(CXCR7)对小鼠胚胎肝干细胞14-19(HP14-19)增殖、迁移和抗氧化应激损伤的影响。重组腺病毒Ad-CXCR4和Ad-CXCR7感染HP14-19细胞,流式细胞术和Western blot检测细胞膜上CXCR4/CXCR7受体的表达;MTT法检测细胞增殖;Transwell法检测细胞迁移;过氧化氢(H2O2)处理细胞,建立氧化应激损伤模型,MTT法检测细胞活力;酶学法检测乳酸脱氢酶(lactic dehydrogenase,LDH)和超氧化物歧化酶(superoxide dismutase,SOD)活性。结果显示,感染腺病毒Ad-CXCR4/CXCR7后,HP14-19细胞膜CXCR4/CXCR7受体水平显著上调;高表达CXCR7可增强细胞增殖活性,而高表达CXCR4对细胞增殖活性无显著效果;高表达CXCR4或CXCR7可显著增强SDF-1诱导的HP14-19细胞的迁移和氧化应激状态下的细胞存活率,其中,CXCR7对迁移效应较强;与对照组比较,高表达CXCR4或CXCR7可降低H2O2造成的细胞LDH活性,增强SOD活性。因此,CXCR4参与了SDF-1诱导的HP14-19细胞增殖作用,且CXCR4/CXCR7介导SDF-1诱导HP14-19细胞的迁移和抗氧化应激损伤作用。
This study explored the effects of stromal cell-derived factor-1 (SDF-1) / chemotaxis cytokine receptor 4 (CXCR4) and SDF-1 / chemokine cytokines Effect of Receptor 7 (CXCR7) on Proliferation, Migration and Antioxidative Stress Injury in Mouse Embryonic Liver Stem Cells 14-19 (HP14-19). HP14-19 cells were infected with recombinant adenovirus Ad-CXCR4 and Ad-CXCR7, the expression of CXCR4 / CXCR7 receptor was detected by flow cytometry and Western blot, the proliferation of cells was detected by MTT assay, the migration of cells was detected by Transwell assay, H2O2). The oxidative stress injury model was established. The cell viability was detected by MTT assay. The activities of lactic dehydrogenase (LDH) and superoxide dismutase (SOD) were detected by enzyme-linked immunosorbent assay. The results showed that the expression of CXCR4 / CXCR7 receptor in HP14-19 cells was significantly up-regulated after adenovirus Ad-CXCR4 / CXCR7 infection, CXCR7 increased the cell proliferation activity, and CXCR4 was no significant effect on cell proliferation; Or CXCR7 could significantly enhance the migration of SDF-1-induced HP14-19 cells and the cell survival rate under oxidative stress. Among them, CXCR7 had a strong effect on migration; compared with the control group, high expression of CXCR4 or CXCR7 could reduce the H2O2 production Of cells LDH activity, enhance SOD activity. Therefore, CXCR4 is involved in the proliferation of HP14-19 cells induced by SDF-1, and CXCR4 / CXCR7 mediates SDF-1-induced HP14-19 cell migration and anti-oxidative stress injury.