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目的:研究rhIL-1α与1,25-(OH)2D3联合作用对HPDLFs表达RANKL和OPG的影响,探讨牙槽骨改建的调节机制。方法:10μg/L rhIL-1α与1×10-8 mol/L1,25-(OH)2D3联合作用于体外培养的HPDLFs,于48h后收集细胞,利用荧光定量RT-PCR技术检测RANKL mRNA和OPG mRNA的表达,探讨RANKL/OPG比值的变化。结果:rhIL-1α和1,25-(OH)2D3都调节HPDLFs表达RANKL和OPG。rhIL-1α单独作用上调HPDLFs表达RANKL和OPG,增加RANKL/OPG比值(P<0.05);1,25-(OH)2D3单独作用则上调表达RANKL,下调表达OPG,增加RANKL/OPG比值(P<0.05)。这2种调节因子联合作用对HPDLFs RANKL表达有协同作用,但对RANKL/OPG比值的影响无协同效应。结论:rhIL-1α和1,25-(OH)2D3都通过RANKL-OPG途径调节HPDLFs参与牙槽骨改建,2种调节因子联合作用对RANKL表达的影响明显优于单因素诱导效果,但对RANKL/OPG比值的影响并没有产生协同效应或累加效应。
AIM: To investigate the effect of rhIL-1α and 1,25- (OH) 2D3 on the expression of RANKL and OPG in HPDLFs and to explore the regulatory mechanism of alveolar bone remodeling. Methods: HPDLFs cultured in vitro were treated with 10μg / L rhIL-1α and 1 × 10-8 mol / L, 25- (OH) 2D3. Cells were harvested after 48h. Fluorescent quantitative RT-PCR was used to detect RANKL mRNA and OPG mRNA expression, to explore the RANKL / OPG ratio changes. Results: Both rhIL-1α and 1,25- (OH) 2D3 regulated the expression of RANKL and OPG in HPDLFs. The effect of rhIL-1α alone was upregulated in HPDLFs expressing RANKL and OPG, and the ratio of RANKL / OPG was increased (P <0.05); 1,25- (OH) 2D3 alone increased expression of RANKL, down-regulated expression of OPG and increased RANKL / 0.05). The combination of these two regulators had a synergistic effect on the expression of RANKL in HPDLFs, but had no synergistic effect on the ratio of RANKL / OPG. CONCLUSION: Both rhIL-1α and 1,25- (OH) 2D3 regulate the expression of HPDLFs in alveolar bone through the RANKL-OPG pathway. The combined effect of the two regulators on RANKL expression is significantly better than the single factor-induced effect, / OPG ratio did not produce synergistic effects or additive effects.