The Third Department of Orthopedics, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Rheumatol Int. 2012 Nov;32(11):3669-73. doi: 10.1007/s00296-011-2091-8. Epub 2011 Sep 7.
Here, we used glucocorticoid as an apoptosis inducer to study how glucocorticoid could accelerate cartilage degeneration and the responsible signal pathway. Human chondrocytes were isolated from knee joints gave glucocorticoid of different concentrations for 24 h, 48 h, 72 h, or 1 week, and cell viability was determined. Next, Sox9, Collagen type II, Aggrecan protein expression and mRNA transcription were detected by western blot analysis and quantitative real-time PCR, respectively. Glucocorticoid could suppress chondrocyte growth at the concentration of 100 μM. When cultured with glucocorticoid, the expressions of Sox9, Col II, and Aggrecan were depressed time-dependent and dose-dependent, as well as the mRNA transcription. The glucocorticoid-induced p38 inactivation was one mechanism that may response for the inhibition of extracellular matrix synthesis, and these influences appeared earlier than the apoptosis effect.
在这里,我们使用糖皮质激素作为凋亡诱导剂来研究糖皮质激素如何加速软骨退化以及负责的信号通路。我们从膝关节分离出人软骨细胞,给予不同浓度的糖皮质激素 24 小时、48 小时、72 小时或 1 周,并测定细胞活力。然后,通过 Western blot 分析和定量实时 PCR 分别检测 Sox9、Collagen type II、Aggrecan 蛋白表达和 mRNA 转录。糖皮质激素在 100 μM 的浓度下可以抑制软骨细胞生长。用糖皮质激素培养时,Sox9、Col II 和 Aggrecan 的表达呈时间和剂量依赖性下降,mRNA 转录也是如此。糖皮质激素诱导的 p38 失活可能是抑制细胞外基质合成的一种机制,而且这些影响出现在凋亡作用之前。