cAMP-PKA途径在小鼠受精卵卵裂中的作用

目的：探讨环腺苷酸-蛋白激薄A(cAMP—PKA)途径在小鼠受精卵早期卵裂中的变化规律及作用。方法：动态观察小鼠1—细胞期受精卵M期cAMP浓度及PKA、成熟作用促进因子(MPF)活性变化。并应用cAMP及蛋白激酶抑制剂(PKI)显微注射入1-细胞期受精卵内，观察卵细胞形态学变化及卵裂率、死亡率。结果：小鼠受精卵1-细胞期，伴随MPF活性变化，M期cAMP浓度下降，M中期最低，M末期升高，与PKA趋势一致。cAMP显微注射后卵细胞胞膜及透明带变形，形态不规则，无卵裂发生；PKI显微注射后核不规则分裂增加，正常卵裂率下降。两者死亡率均高于对照组。结论：cAMP注射升高PKA活性可使卵细胞发育迟缓，PKI注射抑制PKA活性引起核不规则分裂。

Effect of cAMP-PKA Pathway on Cleavage of Fertilized Eggs in Mice

Objective: Our aim was to study the effect of protein kinase A (PKA) on cell cycle progression on cleavage of fertilized eggs of mice. Methods: Cyclic adenosine monophosphate (cAMP) concentration, PKA, and activity of maturation promoting factor (MPF) were determined. Morphological changes and percentage of cleavage or death were observed after microinjection of PKA stimulator cAMP and protein kinase inhibitor (PKI) into 1-cell stage fertilized eggs of mice. Results: The concentration of cAMP and the activity of PKA decreased at the onset of mitosis and increased at the transition from mitosis to interphase. The cAMP, as the stimulator of PKA, could inhibit embryos division; while PKI, the inhibitor of PKA, induced irregular division of fertilized eggs. Both cAMP and PKI increased the percentage of cell death. Conclusion: The cAMP-PKA pathway can influence the cleavage of fertilized eggs in mice.