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前列腺素E2(prostaglandin E2,PGE2)作为细胞因子,在骨代谢中扮演重要角色.它通过刺激成骨细胞核因子κB受体活化因子配基(receptor activator of nuclear factor kappa B ligand,RANKL)表达,促进破骨细胞的分化成熟.然而,其是否参与了电磁场调节骨代谢仍不清楚.PGE2的生物合成受到环加氧酶(cyclooxygenase,COX)的调节.在细胞中存在2种不同的环加氧酶,COX-1和COX-2.其中,COX-2是引起PGE2分泌增加的主要原因.其活性受到细胞核因子κB(nuclear factor kappa B,NF-κB)的调节.本文通过检测体外培养成骨细胞PGE2分泌,COX-2蛋白表达以及Cox-2、Opg、Rankl和Nf-κb基因表达发现,经50 Hz 1.8 m T正弦交变电磁场(sinusoidal electromagnetic fields,SEMFs)处理后,由COX-2介导的PGE2分泌以及cox-2、Nf-κb的基因表达皆下调,但Nf-κb的变化先于cox-2的变化,而opg/rankl基因表达则恰恰相反,说明电磁场通过抑制Nf-κb的转录降低由COX-2介导的PGE2的分泌,进而降低对Rankl表达的刺激作用,抑制破骨细胞的分化成熟.
Prostaglandin E2 (PGE2), as a cytokine, plays an important role in bone metabolism by promoting the expression of receptor activator of nuclear factor kappa B ligand (RANKL) However, it remains unclear whether it participates in the regulation of bone metabolism by electromagnetic field.PGE2 biosynthesis is regulated by cyclooxygenase (COX), there are two kinds of cyclooxygenase , COX-1 and COX-2, among which, COX-2 is the main reason for the increase of PGE2 secretion.Its activity is regulated by nuclear factor kappa B (NF-κB) PGE2 secretion, expression of COX-2 protein and expression of Cox-2, Opg, Rankl and Nf-κb genes were detected by COX-2 after treatment with 50 Hz 1.8 m T sinusoidal electromagnetic fields (SEMFs) PGE2 secretion and cox-2, Nf-κb gene expression were down-regulated, but Nf-κb changes before cox-2 changes, and opg / rankl gene expression is exactly the opposite, indicating that the electromagnetic field through the inhibition of Nf-κb transcription Reduce PGE2 mediated by COX-2 Secretion, thereby reduce the stimulation of Rankl expression, inhibit the differentiation of osteoclast maturation.