目的探讨miR-145对间充质来源软骨细胞肥大化的调控作用。方法用肥大化完全诱导培养基对间充质干细胞进行软骨细胞肥大化诱导,检测肥大化相关基因表达,确定间充质来源软骨细胞肥大化诱导成功。实验分为转染antagomiR-145(miRNA拮抗剂)组和对照组,应用qRT-PCR检测miR-145对软骨细胞肥大化标志基因Ⅹ型胶原(ColⅩ)、成纤维细胞生长因子受体-1(FGFR-1)和基质金属蛋白酶-13(MMP-13)转录水平的影响。结果转染antagomiR-145可以延缓间充质来源软骨细胞肥大化进程。转染antagomiR-145后肥大化软骨细胞的标志物ColⅩ、FGFR-1、MMP-13的表达量与对照组相比显著降低(P<0.05),而ColⅡ的表达与对照组相比显著增多(P<0.05)。结论抑制miR-145的表达能有效地延缓间充质干细胞向肥大化软骨细胞分化进程。 Objective To investigate the regulatory effect of miR-145 on the hypertrophy of mesenchymal-derived chondrocytes. Methods The hypertrophy of complete induction medium was used to induce chondrocyte hypertrophy in mesenchymal stem cells. The expression of genes related to hypertrophy was detected to confirm the successful induction of mesenchymal-derived chondrocytes. The experiment was divided into antagomiR-145 (miRNA antagonist) group and control group. QRT-PCR was used to detect the effect of miR-145 on the expression of chondrocyte marker gene Ⅹcollagen, fibroblast growth factor receptor-1 FGFR-1) and matrix metalloproteinase-13 (MMP-13) transcription levels. Results Transfection of antagomiR-145 delayed the process of mesenchymal-derived chondrocyte hypertrophy. The expression of ColX, FGFR-1 and MMP-13 in transfected antagomiR-145 cells was significantly lower than that in the control group (P <0.05), while the expression of ColⅡ was significantly increased compared with the control group P <0.05). Conclusion Inhibition of miR-145 expression can effectively delay the process of mesenchymal stem cells differentiating into hypertrophic chondrocytes.