地塞米松磷酸钠对兔关节软骨细胞体外培养的影响

Effects of dexamethasone sodium phosphate on rabbit articular chondrocytes cultured in vitro

目的探讨地塞米松磷酸钠对体外培养兔关节软骨细胞的影响。方法兔关节软骨细胞常规培养后随机分为对照组和实验组,对照组用不含地塞米松磷酸钠的DMEM培养液培养,实验组则分别加入含不同浓度地塞米松磷酸钠的DMEM培养液,应用流式细胞术及免疫细胞化学法检测软骨细胞增殖情况及其合成Ⅱ型胶原能力,并应用透射电子显微镜观察软骨细胞超微结构的变化。结果实验各组软骨细胞进入S期、G2+M期的细胞比率较对照组软骨细胞减少、进入G0/G1期的细胞比率增加,免疫细胞化学阳性信号的平均灰度值与对照组平均灰度值的差异均有显著性,电镜下见软骨细胞线粒体、粗面内质网数量减少。结论地塞米松磷酸钠可抑制软骨细胞的增殖,可能与抑制关节软骨细胞的Ⅱ型胶原和蛋白合的合成能力有关。

Objective To investigate the effects of dexamethasone sodium phosphate on proliferation of rabbit articular chondrocytes cultured in vitro , Methods Rabbit articular chondrocytes cultured in vitro were divided randomly into four groups. Cells of the control group were cultured in DMEM media without dexamethasone sodium phosphate ; cells of exper/meutal groups were cultured in DMEM media with different concentration of dexamethasone sodium phosphate respectively, Flow ,cytometry and immunocytochemistry were used to observe the effect of dexamethasone sodium phosphate orr proliferation of chondrocytes and synthesis of type Ⅱ collagen . The changes of ultrastructure of cultured chondrocytes were observed under transmission electron microscope. Results The cellular proportions of S period and G2^＋ M period of the experimental groups decreased and the cellular proportions of G0/G1 period inereased. There were significant differences between the average gray scale values of the experimental groups and those of the control group. Under transmission electron microscope the amount of rough surfaced end oplasmic reticula and mitochondria of the experimental groups decreased. Conclusion Dexamethasone sodium phosphate can inhibit the prolifreation of articular ehondroeyte. The enhanced proliferation of ehondrocyte may be due to the decrease of cellular proportions of S period. Dexamethasone sodium phosphate can inhibit the synthesis of type Ⅱ collagen and protein of ehondroeytes. The injection of dexamethasone sodium phosphate into articular cavity may result in impairemen of articular cartilage and may accelerate the retrogrde degeneration of articular cartilage.