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高浓度地塞米松通过下调LMP-1表达抑制大鼠成骨细胞的分化

刘素彩, 张志勇, 李恩

河北医科大学生物化学教研室,石家庄(050017)；石家庄市第四医院,石家庄(050011)

摘要

为探讨地塞米松（dexamethasone，DEX）抑制成骨细胞分化的机制，观察了不同浓度DEX对体外培养大鼠成骨细胞的碱性磷酸酶活性、骨钙素（osteocalcin，OC）合成、I型胶原蛋白表达的影响，并用RT-PCR方法检测了成骨细胞中LIM矿化蛋白1 mRNA的表达量。结果显示：低浓度（10~(-9)mol/L）的DEX能增加碱性磷酸酶的活性、OC的分泌和I型胶原蛋白的表达；而高浓度（10~(-7)mol/L）的DEX对它们则起抑制作用，并不调成骨细胞正调节因子LMP-1 mRNA的表达。上述结果表明，低浓度的DEX促进成骨细胞的分化；高浓度的DEX则抑制成骨细胞的分化，其抑制作用可能是通过下调LMP-1 mRNA的表达而实现的。

关键词： 地塞米松; LIM矿化蛋白1表达; 成骨细胞分化

Dexamethasone inhibits osteoblastic differentiation by down-regulation of LIM mineralization protein 1

Liu Sucai, Zhang Zhiyong, Li En

Department of Biochemistry, Hebei Medical University,Shijiazhuang(050017)；The Fourth Hospital of Shijiazhuang,Shijiazhuang(050011)

Abstract

To investigate the mechanisms of the inhibition of osteoblastic differentiation by dexamethasone (DEX), the effects of different doses of DEX on the activity of alkaline phosphatase (ALP), the synthesis of osteocalcin (OC) and the expression of colaggen type I were observed in the cultured rat osteoblasts. THe LIM mineralization protein-1 (LMP-1) mNRA, a positive regulator of osteoblasts, was semi-quantified by RT-PCR. The results showed that a lower dose (10~(-9)mol/L) of DEX could enhance the activity of ALP, the synthesis of OC and the expression of collagen type I. However, a higher dose (10~(-7)mol/L) of DEX inhibited them and down-regulated the expression of LMP-1 mRNA in osteoblasts. It is suggested that DEX stimulates osteoblast differentiation at lower dose, while at higher dose it inhibits osteoblast differentiation. The inhibitory action of DEX on osteoblast differentiation might be mediated by the down-regulation of LMP-1 mRNA.

Key words: Dexa methasone;LIM mineralization protein 1 expression;Osteoblastic differentiation

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引用本文：

刘素彩, 张志勇, 李恩. 高浓度地塞米松通过下调LMP-1表达抑制大鼠成骨细胞的分化[J]. 生理学报 2002; 54 (1): .

Liu Sucai, Zhang Zhiyong, Li En. Dexamethasone inhibits osteoblastic differentiation by down-regulation of LIM mineralization protein 1. Acta Physiol Sin 2002; 54 (1): (in Chinese with English abstract).