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目的 探讨脆性X智力低下一号基因 (FMR1)表达缺失对环磷酸腺苷 (cAMP)的影响及其机制。方法 通过硝普钠封闭FMR1,建立脆性X综合征细胞模型 ;研究FMR1表达缺失对cAMP水平及cAMP代谢途径中的两个关键酶 [腺苷酸环化酶 (AC)及磷酸二酯酶 (PDE) ]活性的影响。结果 在细胞水平 ,硝普钠可成功地封闭FMR1基因 ;基因封闭组细胞内cAMP水平明显低于对照组 (P =0 0 0 0 ) ;该组腺苷酸环化酶的比活力明显低于对照组 (P =0 0 0 0 ) ,而磷酸二酯酶比活力则无显著改变(P =0 983)。结论 FMR1基因表达缺失可导致细胞内cAMP的水平降低 ,腺苷酸环化酶活性被抑制可能是其降低的原因之一。
Objective To investigate the effect of FMR1 deficiency on cAMP and its mechanism. Methods Fragile X syndrome cell model was established by sodium nitroprusside blocking FMR1. The effects of FMR1 expression loss on cAMP level and two key enzymes in cAMP pathway [adenylate cyclase (AC) and phosphodiesterase (PDE) )] Activity. Results At the cellular level, sodium nitroprusside could successfully block the FMR1 gene. The level of cAMP in the gene-blocked group was significantly lower than that in the control group (P = 0.0000). The specific activity of adenylate cyclase was significantly lower The control group (P = 0 0 0 0), while phosphodiesterase specific activity was not significantly changed (P = 0 983). Conclusion The lack of FMR1 gene expression may lead to the decrease of intracellular cAMP levels and the inhibition of adenylate cyclase activity may be one of the reasons for its decrease.