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目的探讨炎性微环境中糖原合成酶激酶-3β(GSK-3β)对颌骨来源间充质干细胞(JBMMSCs)成骨分化的影响。方法应用慢病毒(sh RNA)转染技术在JBMMSCs中敲减GSK-3β表达,利用白细胞介素(IL)-1β和肿瘤坏死因子(TNF)-α模拟炎症微环境。成骨诱导后利用Western Blot检测成骨相关蛋白表达,茜素红染色检测成骨效率。结果敲减GSK-3β表达可增强JBMMSCs成骨诱导后的成骨相关蛋白表达,成骨效率增强。炎症微环境可显著下调正常JBMMSCs成骨诱导后的成骨相关蛋白表达,成骨效率明显降低,而对敲减GSK-3β表达的JBMMSCs成骨诱导后的成骨相关蛋白表达下调较弱,成骨效率降低较轻。结论抑制GSK-3β既可促进JBMMSCs的成骨作用,又可减轻炎性微环境对JBMMSCs成骨的不良影响,为提高炎症状态下JBMMSCs促进组织再生提供了新的治疗靶点。
Objective To investigate the effect of glycogen synthase kinase-3β (GSK-3β) on the osteogenic differentiation of bone marrow-derived mesenchymal stem cells (JBMMSCs) in inflammatory microenvironment. Methods The expression of GSK-3β was knocked down in JBMMSCs by sh RNA transfection. The inflammatory microenvironment was modeled by interleukin (IL) -1β and tumor necrosis factor (TNF) -α. Osteogenesis-related protein expression was detected by Western Blot after osteogenic induction, and osteogenic efficiency was detected by alizarin red staining. Results The knockdown of GSK-3β expression enhanced the osteogenesis-related protein expression induced by osteogenesis in JBMMSCs, and the osteogenesis efficiency was enhanced. The inflammation microenvironment could significantly down-regulate the osteogenesis-related protein expression induced by osteogenesis in normal JBMMSCs, and the osteogenesis efficiency was significantly reduced. However, the down-regulation of osteogenesis-related protein expression in osteogenesis induced by GSK-3β knockdown was weaker Bone reduction is less effective. Conclusion Inhibition of GSK-3β can not only promote the osteogenesis of JBMMSCs, but also reduce the adverse effects of inflammatory microenvironment on the osteogenesis of JBMMSCs. It provides a new therapeutic target for enhancing the tissue regeneration of JBMMSCs under inflammatory conditions.