Imai A, Iida K, Tamaya T
Department of Obstetrics and Gynecology, Gifu University School of Medicine, Japan.
Arch Gynecol Obstet. 1991;248(3):117-21. doi: 10.1007/BF02390088.
The mechanisms by which gonadotropin-releasing hormone (LH-RH) analogue buserelin exerts direct action on the ovary was investigated. The analogue inhibited the luteinizing hormone (LH)-induced increase of steroidogenesis by rat ovarian granulosa cells in a dose-dependent manner. The LH-RH analogue did not alter binding capacity and affinity of 125I-LH to granulosa cells, suggesting the involvement of post-receptor mechanism. Likewise, the analogue caused inositol trisphosphate (IP3) formation as a result of stimulated inositol-phospholipid turnover. Half maximal effects of both steroidogenesis suppression and IP3 production occurred at 10 nM buserelin. These findings indicate that the inhibitory action of buserelin on granulosa cell function is mediated by IP3 (or calcium)-dependent mechanisms. Buserelin, in addition to its well-known action at pituitary level, exerts a direct inhibition of ovarian steroidogenesis at gonadal level without changes in gonadotropin receptors.
研究了促性腺激素释放激素（LH-RH）类似物布舍瑞林对卵巢发挥直接作用的机制。该类似物以剂量依赖的方式抑制促黄体生成素（LH）诱导的大鼠卵巢颗粒细胞类固醇生成增加。LH-RH类似物未改变125I-LH与颗粒细胞的结合能力和亲和力，提示其作用涉及受体后机制。同样，该类似物因刺激肌醇磷脂代谢而导致肌醇三磷酸（IP3）形成。布舍瑞林抑制类固醇生成和产生IP3的半数最大效应均在10 nM时出现。这些发现表明，布舍瑞林对颗粒细胞功能的抑制作用是由IP3（或钙）依赖性机制介导的。布舍瑞林除了在垂体水平具有众所周知的作用外，还在性腺水平对卵巢类固醇生成发挥直接抑制作用，而不改变促性腺激素受体。
