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[猪血管活性肠肽对培养的小鼠卵母细胞减数分裂的抑制作用]

[An inhibitory influence of porcine vasoactive intestinal peptide upon mouse oocyte meiosis in culture].

作者信息

Sato E

机构信息

Department of Animal Science, Faculty of Agriculture, Kyoto University, Japan.

出版信息

Nihon Naibunpi Gakkai Zasshi. 1990 Jan 20;66(1):22-8. doi: 10.1507/endocrine1927.66.1_22.

Abstract

The germinal vesicle (GV) of follicle-enclosed oocytes in mice remains arrested at the dictyate state of meiosis. Upon releasing the oocytes from the follicles, the meiotic process resumes, leading to dissolution of the GV, suggesting that factors in the follicular constituents sustain the meiotic arrest of oocytes. Vasoactive intestinal peptide (VIP) was demonstrated in the ovary and found to have a wide range of biological effects. In this study, the possibility of VIP to be a factor which induces meiosis-arrest of oocytes was evaluated. Porcine VIP inhibited resumption of meiosis of cumulus-enclosed mouse oocytes in vitro. Germinal vesicle breakdown (GVBD) was prevented in more than 50% of the oocytes treated by VIP at a concentration of 30 microM. The inhibiting effect of VIP was dose-dependent and reversible. Spontaneous resumption of meiosis of isolated oocytes in vitro was reported to be inhibited by dibutyryl cAMP (dbcAMP) added to the medium, indicating that meiotic arrest can be sustained by maintaining intra-oocyte cAMP above a critical level. It was further reported that follicular fluid contains substances that maintain meiotic arrest in association with exogenous dbcAMP. In the present study, the blocking activity of dbcAMP for the spontaneous resumption of meiosis was not potentiated by the addition of VIP in the medium. The present results suggest that VIP may play a role in the regulation of resumption of oocyte meiosis, and that VIP is not a substance which maintains meiotic arrest in association with cAMP.

摘要

小鼠卵泡内包裹的卵母细胞的生发泡(GV)停滞于减数分裂的双线期。将卵母细胞从卵泡中释放后,减数分裂过程恢复,导致生发泡溶解,这表明卵泡成分中的因子维持了卵母细胞的减数分裂停滞。血管活性肠肽(VIP)在卵巢中被证实存在,并被发现具有广泛的生物学效应。在本研究中,评估了VIP作为诱导卵母细胞减数分裂停滞因子的可能性。猪VIP在体外抑制了卵丘包裹的小鼠卵母细胞减数分裂的恢复。在浓度为30微摩尔的VIP处理的卵母细胞中,超过50%的卵母细胞阻止了生发泡破裂(GVBD)。VIP的抑制作用呈剂量依赖性且可逆。据报道,添加到培养基中的二丁酰环磷腺苷(dbcAMP)可抑制体外分离的卵母细胞自发恢复减数分裂,这表明通过将卵母细胞内的cAMP维持在临界水平以上可维持减数分裂停滞。进一步报道称,卵泡液含有与外源性dbcAMP相关的维持减数分裂停滞的物质。在本研究中,培养基中添加VIP并未增强dbcAMP对减数分裂自发恢复的阻断活性。目前的结果表明,VIP可能在卵母细胞减数分裂恢复的调节中起作用,并且VIP不是一种与cAMP相关维持减数分裂停滞的物质。

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