• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

人绒毛膜促性腺激素未能逆转大鼠卵巢卵泡颗粒细胞中诱导的初期闭锁变化。

Failure of hCG to reverse incipient atretic changes induced in granulosa cells of rat ovarian follicles.

作者信息

Parshad R K

机构信息

Department of Zoology, Punjab Agricultural University, Ludhiana, India.

出版信息

Indian J Exp Biol. 1994 Feb;32(2):86-8.

PMID:8045618
Abstract

Surface membrane changes in the granulosa cells from follicles at different times following a single dose of PMSG have been investigated after the incubation of cells in media with and without hCG by spectrophotometric measure of concanavalin A-induced cellular agglutination rate. Agglutination rate and final level of agglutination of cells do not change from 24 to 48 hr but significantly rise at 72, 96 and 120 hr after PMSG administration. Incubation of cells in presence of hCG for 20 min decrease the agglutination level of cells at 24, 48 and 72 hr and no significant change was observed at 96 and 120 hr. The results, thus suggest that atretic changes when induced in the surface membrane of granulosa cells (after 72 hr of PMSG administration) cannot be reversed with hCG.

摘要

通过分光光度法测定伴刀豆球蛋白A诱导的细胞凝集率,研究了在给予单剂量孕马血清促性腺激素(PMSG)后不同时间卵泡颗粒细胞的表面膜变化。在含有和不含人绒毛膜促性腺激素(hCG)的培养基中培养细胞后发现,细胞的凝集率和最终凝集水平在PMSG给药后24至48小时内没有变化,但在72、96和120小时时显著升高。在hCG存在的情况下将细胞孵育20分钟,可降低24、48和72小时时细胞的凝集水平,而在96和120小时时未观察到显著变化。因此,结果表明,颗粒细胞表面膜诱导的闭锁变化(PMSG给药72小时后)不能被hCG逆转。

相似文献

1
Failure of hCG to reverse incipient atretic changes induced in granulosa cells of rat ovarian follicles.人绒毛膜促性腺激素未能逆转大鼠卵巢卵泡颗粒细胞中诱导的初期闭锁变化。
Indian J Exp Biol. 1994 Feb;32(2):86-8.
2
Hormonal induction of ovulation stimulates atresia of antral follicles in a vespertilionid bat, Scotophilus heathi.激素诱导排卵会刺激一种蝙蝠(印度黄蝠)的窦状卵泡闭锁。
Zoology (Jena). 2006;109(3):208-16. doi: 10.1016/j.zool.2006.02.001. Epub 2006 Jun 30.
3
Progesterone receptor activation mediates LH-induced type-I pituitary adenylate cyclase activating polypeptide receptor (PAC(1)) gene expression in rat granulosa cells.孕酮受体激活介导促黄体生成素诱导大鼠颗粒细胞中I型垂体腺苷酸环化酶激活多肽受体(PAC(1))基因的表达。
Biochem Biophys Res Commun. 2000 Oct 14;277(1):270-9. doi: 10.1006/bbrc.2000.3667.
4
Chemotactic detection of incipient ovarian follicular atresia.早期卵巢卵泡闭锁的趋化检测
Indian J Exp Biol. 1992 Jan;30(1):5-7.
5
Expression of mitochondria-dependent apoptosis genes (p53, Bax, and Bcl-2) in rat granulosa cells during follicular development.大鼠卵泡发育过程中颗粒细胞中线粒体依赖性凋亡基因(p53、Bax和Bcl-2)的表达
J Soc Gynecol Investig. 2004 Jul;11(5):311-7. doi: 10.1016/j.jsgi.2004.01.015.
6
Follicular atresia as an apoptotic process: atresia-associated increase in the ovarian expression of the putative apoptotic marker sulfated glycoprotein-2.卵泡闭锁作为一种凋亡过程:闭锁相关的假定凋亡标志物硫酸化糖蛋白-2在卵巢中的表达增加。
J Soc Gynecol Investig. 1996 Jul-Aug;3(4):199-208.
7
Induction of alpha-caveolin-1 (alphaCAV1) expression in bovine granulosa cells in response to an ovulatory dose of human chorionic gonadotropin.人绒毛膜促性腺激素排卵剂量刺激下牛颗粒细胞中α-小窝蛋白-1(αCAV1)表达的诱导。
Mol Reprod Dev. 2006 Nov;73(11):1353-60. doi: 10.1002/mrd.20513.
8
Cumulus cells of oocyte-cumulus complexes secrete a meiosis-activating substance when stimulated with FSH.卵母细胞-卵丘复合体的卵丘细胞在受到促卵泡激素刺激时会分泌一种减数分裂激活物质。
Mol Reprod Dev. 1997 Mar;46(3):296-305. doi: 10.1002/(SICI)1098-2795(199703)46:3<296::AID-MRD8>3.0.CO;2-K.
9
Clusterin protects granulosa cells from apoptotic cell death during follicular atresia.簇集素在卵泡闭锁过程中保护颗粒细胞免于凋亡性细胞死亡。
Exp Cell Res. 2000 May 25;257(1):101-10. doi: 10.1006/excr.2000.4885.
10
DNA degradation in mural granulosa cells of non- and slightly atretic follicles of fresh and cold-stored domestic cat ovaries.新鲜和冷藏家猫卵巢中非闭锁和轻度闭锁卵泡壁颗粒细胞中的DNA降解
Mol Reprod Dev. 1997 Nov;48(3):350-5. doi: 10.1002/(SICI)1098-2795(199711)48:3<350::AID-MRD8>3.0.CO;2-Q.