胰岛素样生长因子-Ⅰ在体外对人卵巢颗粒细胞雌二醇和孕酮产生量及超微结构的影响

The Effect of Insulin-like Growth FactorI on Steroidogenesis and Ultrastructures of Cultured Human Granulosa Cells in Vitro

目的观察胰岛素样生长因子－Ⅰ（ＩＧＦ－Ⅰ）在体外对人卵巢颗粒细胞雌二醇（Ｅ２）和孕酮（Ｐ）产生量及超微结构的影响，及其与促卵泡激素（ＦＳＨ）的关系。方法培养人卵巢颗粒细胞，以终浓度为０．１３、１．３１、６．５３和１３．０７ｎｍｏｌ／Ｌ的ＩＧＦ－Ⅰ及６．５３ｎｍｏｌ／Ｌ的ＩＧＦ－Ⅰ＋０．１５ｎｍｏｌ／Ｌ的ＦＳＨ分别对其刺激，对照组不加ＩＧＦ－Ⅰ及ＦＳＨ，用放射免疫法检测颗粒细胞Ｅ２和Ｐ产生量，同时对ＩＧＦ－Ⅰ浓度为６．５３ｎｍｏｌ／Ｌ组及对照组颗粒细胞作透射电子显微镜检查。结果Ｅ２产生量分别为４３．９、５９．５、８７．３和９２．８ｐｍｏｌ／１０００细胞（对照组为３０．１ｐｍｏｌ／１０００细胞），Ｐ产生量分别为３．４、７．６、１３．９和１４．６ｎｍｏｌ／１０００细胞（对照组为１．０ｐｍｏｌ／１０００细胞），均明显高于对照组（Ｐ＜０．０１）。ＩＧＦ－Ⅰ和ＦＳＨ共同刺激后，Ｅ２和Ｐ产生量较单纯ＦＳＨ刺激分别增加３．５倍和１４．５倍（Ｐ＜０．０１）。经ＩＧＦ－Ⅰ刺激后，颗粒细胞超微结构与对照组比较有明显差异，主要表现为线粒体和滑面内质网非常丰富，胞质内有大量脂滴。结论经ＩＧＦ－Ⅰ刺激后，颗粒细胞超微结构向有利于雌、孕?

Objective To observe the effect of insulinlike growth factorⅠ (IGFⅠ) on steroidogenesis and ultrastructures of cultured human granulosa cells in vitro and the synergetic influence of follicle stimulating hormone (FSH) on this process. Methods Human granulosa cells were cultured in serumfree 1640 medium. After stimulated with various concentrations of IGFⅠ or IGFⅠ+FSH for 24 hours, estradiol (E2) and progesterone (P) levels in the media were measured by radioimmunoassay, and the ultrastructure changes of granulosa cells were observed under electronic microscope. Resutls When stimulated with different concentrations of IGFⅠfor 24 hours, E2 and P levels produced by granulosa cells were in a dosedependent manner and significantly higher than those of controls (P<0.01). The E2 and P levels in the media under the stimulation of IGFⅠ+FSH were 3.5 times and 14.5 times respectively higher than those of FSH alone. The main ultrastructureal appearences of granulosa cells stimulated with IGFⅠwere abundance of enlarged smooth enodplasmic reticulum, mitochondria and lipid droplets in cytoplasm. Conclusions IGFⅠ possesses a positive effect on the steroidogenesis of cultured human granulosa cells in dosedependent fashion which could be enhanced by combination of IGFⅠ and FSH. The ultrastructures of granulosa cells showed a tendency toward activation of steroidogenesis under the stimulation of IGFⅠ.