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血管紧张素II对仓鼠卵巢卵泡类固醇生成及卵泡膜内层超微结构的体外作用。

In-vitro effects of angiotensin II on steroid production by hamster ovarian follicles and on ultrastructure of the theca interna.

作者信息

Kitzman P H, Hutz R J

机构信息

Department of Cell Biology, Neurobiology, and Anatomy, Ohio State University, Columbus 43210-1239.

出版信息

Cell Tissue Res. 1992 Apr;268(1):191-6. doi: 10.1007/BF00338068.

Abstract

Angiotensin II (AII) is present in the mammalian ovary and has been correlated with atresia in follicles. Since the theca interna may be one site at which atresia is initiated, we wished to determine whether AII exerts an effect on theca interna from explanted ovarian follicles of hamsters. Hamsters were sacrified on the morning of proestrus, and ovaries were removed. Preovulatory follicles were excised from the ovaries, and cultured with one of the following components: medium alone (control); medium plus AII (1 x 10(-6) M); the AII-receptor antagonist [Sar1, Ile8] AII (1 x 10(-4) M); or AII plus antagonist. After 72 h, the follicles were processed for transmission electron microscopy (to determine quantities of theca interna organelles involved in the steroid synthetic pathway) or for protein determination (to normalize steroid production rates). The incubation medium was drawn off and analyzed by radioimmunoassay for progesterone, androstenedione, or estradiol-17 beta. There was a significant positive correlation (r = 0.92, P less than 0.01) between follicular androstenedione secretion and area comprising theca interna smooth endoplasmic reticulum. In the theca interna, AII induced a two-fold and 1.6-fold increase in lipid droplet number and area comprising smooth endoplasmic reticulum, respectively (P less than 0.05). Excess antagonist negated the increase in cell organelles and also reduced androstenedione secretion compared with AII alone (P less than 0.05). Most importantly, AII significantly augmented the ratio of androstenedione:estradiol-17 beta secretion by 44% over that of control. The ultrastructural changes observed in this study and the increase in the androstenedione:estradiol-17 beta production ratio are consistent with atresia-like changes in ovarian follicles.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

血管紧张素II(AII)存在于哺乳动物卵巢中,且与卵泡闭锁相关。由于卵泡内膜可能是闭锁起始的部位之一,我们希望确定AII对仓鼠离体卵巢卵泡的卵泡内膜是否有作用。在动情前期的早晨处死仓鼠,取出卵巢。从卵巢中切下排卵前卵泡,并用以下成分之一进行培养:单纯培养基(对照);培养基加AII(1×10⁻⁶ M);AII受体拮抗剂[Sar1,Ile8]AII(1×10⁻⁴ M);或AII加拮抗剂。72小时后,对卵泡进行处理以用于透射电子显微镜检查(以确定参与类固醇合成途径的卵泡内膜细胞器数量)或蛋白质测定(以标准化类固醇产生率)。吸出培养液,通过放射免疫分析法分析孕酮、雄烯二酮或雌二醇-17β。卵泡雄烯二酮分泌与构成卵泡内膜滑面内质网的面积之间存在显著正相关(r = 0.92,P < 0.01)。在卵泡内膜中,AII分别使脂滴数量和构成滑面内质网的面积增加了两倍和1.6倍(P < 0.05)。与单独使用AII相比,过量的拮抗剂消除了细胞器的增加,还降低了雄烯二酮的分泌(P < 0.05)。最重要的是,与对照相比,AII使雄烯二酮:雌二醇-17β的分泌比例显著增加了44%。本研究中观察到的超微结构变化以及雄烯二酮:雌二醇-17β产生比例的增加与卵巢卵泡闭锁样变化一致。(摘要截于250字)

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