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目的:探讨高糖环境通过抑制CXCR-4对大鼠下颌骨骨髓基质细胞迁移的影响。方法:从Wistar大鼠下颌骨中分离、培养骨髓基质细胞,利用Transwell实验筛选在生理糖浓度(5.5 mmol/L)下的SDF-1最适迁移浓度,检测不同糖浓度(5.5、16.5 mmol/L)条件下SDF-1、AMD3100对细胞迁移能力的影响。利用Western免疫印迹检测不同糖浓度(5.5、16.5 mmol/L)条件下CXCR-4的表达,实时定量PCR检测CXCR-4、MMP-2的m RNA表达。采用SPSS 11.0软件包对数据进行统计学分析。结果:Transwell检测显示,生理糖浓度下,骨髓基质细胞的迁移能力对趋化因子SDF-1呈浓度依赖性;在生理糖浓度下,趋化因子SDF-1的最适浓度为100 ng/m L。高糖环境可抑制骨髓基质细胞的迁移能力。在不同糖浓度下,SDF-1均可明显增强细胞的迁移能力。加入AMD3100后,这种增强趋势受到明显抑制。高糖环境抑制CXCR-4蛋白以及CXCR-4和MMP-2 m RNA表达。结论:高糖环境可以通过抑制CXCR-4的表达来影响大鼠下颌骨骨髓基质细胞在SDF-1/CXCR-4生物轴调控下的定向迁移能力。
Objective: To investigate the effect of high glucose on the migration of rat bone marrow stromal cells by inhibiting CXCR-4. METHODS: Bone marrow stromal cells were isolated and cultured from the mandibular of Wistar rats. The optimum concentration of SDF-1 in physiological glucose (5.5 mmol / L) was screened by Transwell assay. The effects of different concentrations of glucose (5.5,16.5 mmol / L) under the conditions of SDF-1, AMD3100 on cell migration. Western blot was used to detect the expression of CXCR-4 under different glucose concentrations (5.5, 16.5 mmol / L). The mRNA expression of CXCR-4 and MMP-2 was detected by real-time quantitative PCR. Data were analyzed statistically using SPSS 11.0 software package. Results: Transwell assay showed that the migration ability of bone marrow stromal cells was concentration-dependent to chemokine SDF-1 under physiological glucose concentration. Under physiological glucose concentration, the optimum concentration of chemokine SDF-1 was 100 ng / m L. High glucose environment can inhibit the migration of bone marrow stromal cells. At different concentrations of glucose, SDF-1 significantly enhanced cell migration ability. With the addition of AMD3100, this trend of enhancement has been significantly inhibited. High glucose conditions inhibit CXCR-4 protein and CXCR-4 and MMP-2 mRNA expression. CONCLUSION: High glucose environment can affect the directional migration of rat mandibular bone marrow stromal cells under the regulation of SDF-1 / CXCR-4 biological axis by inhibiting the expression of CXCR-4.