中文摘要：

目的 探讨17β-雌二醇下调人成骨细胞CTGF表达的信号转导机制。方法 人成骨细胞分别用10^-8mol／LE2及雌激素受体拮抗剂ICI182780、PKA阻断剂H-89、PKC阻断剂H-7、NF-kB阻断剂PDTC、PKA活化剂forskolin干预24h，采用Northern blotting、Western blotting分析CTGFmRNA、蛋白表达水平的变化。结果 10^-8mol／L雌二醇可明显下调人成骨细胞CTGFmRNA及蛋白的表达；PKA阻断剂H-89可完全阻断雌二醇对CTGF的降调节作用，而雌激素受体拮抗剂ICI182780、PKC阻断剂H-7、NF-kB阻断剂PDTC对雌二醇介导的CTGF降调节无明显作用。PKA活化剂forskohn可明显下调人成骨细胞CTGFmRNA、蛋白的表达，雌二醇组与forskolin组相比，CTGFmRNA、蛋白的水平无明显差异。结论 17β-雌二醇下词人成骨细胞CTGF表达由PKA介导，雌激素核受体、PKC、NF-kB信号转导通路均不参与雌激素介导的CTGF降调节。

英文摘要：

Objective To investigate the mechanisms involved in the inhibitory effect of 17β-estrodiol on connective tissue growth factor （CTGF） in human osteoblasts. Methods Human osteoblasts were exposed to 17β- estrodiol （10^-8 mol/L） with or without estrogen nuclear receptor antagonist ICI182780, PKC antagonist H-7, PKA antagonist H-89, nuclear factor kappa B antagonist PTDC or PKA agonist forskolin for 24 hours. Northern and Western blot were used to detect the changes of CTGF. Results The expression of CTGF mRNA and protein were down regulated by 17β-estrodiol （10^-8 mol/L）,while this effect was abrogated by H-89,a PKA antagonist,and no influence on this effect was observed with ICI182780, PKC antagonist J-7 and PTDC. Forskohn, a PKA agonist, showed similar inhibitory effect as that of estrodiol on the CTGF expression. Conclusions 17β-estrodiol inhibits the CTGF expression via PKA pathway in human osteoblasts.