Liu Y X, Peng X R, Chen Y J, Carrico W, Ny T
State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing.
Hum Reprod. 1997 Dec;12(12):2748-55. doi: 10.1093/humrep/12.12.2748.
This study was conducted to determine whether prolactin (PRL) suppresses gonadotrophin-induced ovulation and disturbs the co-ordinated gene expression of tissue type plasminogen activator (tPA) and plasminogen activator inhibitor type-1 (PAI-1) in rat ovary. Immature female rats were injected with 10 IU pregnant mare's serum gonadotrophin to stimulate follicle growth, and 48 h received different doses of prolactin followed by 7 IU human chorionic gonadotrophin (HCG). The oviducts were examined for the presence of ova, and the amounts of tPA and PAI-1 mRNA present in the ovary were measured at various times after the hormone treatment. PRL had no significant effect on ovarian weight but caused a dose-dependent decrease in ovulation number. In the control animals receiving HCG alone, 13.3 +/- 1.3 (mean +/- SEM) ova/oviduct were found; while in animals receiving HCG plus 50, 100 or 200 microg PRL, the ovulation number was dose-dependently suppressed by 53.6, 66.9 and 76% respectively at 18 h after treatment. PRL suppression of HCG-induced ovulation was time-dependent. By 24 h after treatment, the number of ova in the oviducts in HCG- and HCG plus PRL-treated groups was not significantly different. PRL also suppressed HCG-induced tPA gene expression in a dose- and time-dependent manner. At all time points examined, tPA mRNA content of whole ovaries and granulosa cells (GC) in PRL-treated groups was lower than in the HCG-treated controls. The activities of PAI-1 in ovarian extracellular fluid (OEF) and PAI-1 mRNA in the theca-interstitial cells (TI) in the PRL-treated groups were higher than in the HCG-treated controls. The highest stimulation by PRL of PAI-1 activity in OEF and of PAI-1 mRNA in TI was observed at 9 h and 6 h after HCG treatment respectively. The localization of tPA and PAI-1 antigens in the ovaries was consistent with changes in the mRNA and activity levels. These data suggest that PRL temporarily delays, but does not completely inhibit, HCG-induced ovulation, which may be caused by a suppression of PA-mediated proteolysis.
本研究旨在确定催乳素（PRL）是否会抑制促性腺激素诱导的排卵，并扰乱大鼠卵巢中组织型纤溶酶原激活物（tPA）和纤溶酶原激活物抑制剂-1（PAI-1）的协同基因表达。对未成熟雌性大鼠注射10 IU孕马血清促性腺激素以刺激卵泡生长，48小时后给予不同剂量的催乳素，随后注射7 IU人绒毛膜促性腺激素（HCG）。检查输卵管中是否存在卵子，并在激素处理后的不同时间测量卵巢中tPA和PAI-1 mRNA的含量。PRL对卵巢重量无显著影响，但导致排卵数呈剂量依赖性下降。在仅接受HCG的对照动物中，发现每个输卵管中有13.3±1.3（平均值±标准误）个卵子；而在接受HCG加50、100或200μg PRL的动物中，处理后18小时排卵数分别被剂量依赖性抑制了53.6%、66.9%和76%。PRL对HCG诱导的排卵的抑制作用具有时间依赖性。处理后24小时，HCG处理组和HCG加PRL处理组输卵管中的卵子数量无显著差异。PRL还以剂量和时间依赖性方式抑制HCG诱导的tPA基因表达。在所有检测时间点，PRL处理组全卵巢和颗粒细胞（GC）中的tPA mRNA含量均低于HCG处理的对照组。PRL处理组卵巢细胞外液（OEF）中PAI-1的活性以及卵泡膜间质细胞（TI）中PAI-1 mRNA的含量均高于HCG处理的对照组。分别在HCG处理后9小时和6小时观察到PRL对OEF中PAI-1活性和TI中PAI-1 mRNA的最高刺激作用。tPA和PAI-1抗原在卵巢中的定位与mRNA和活性水平的变化一致。这些数据表明，PRL会暂时延迟但不会完全抑制HCG诱导的排卵这可能是由PA介导的蛋白水解作用受到抑制所致。
