期刊文献+

GnRHa和避孕药保护化疗所致卵巢损伤的比较研究 被引量:8

Comparison study of the prevention of chemotherapy-induced ovarian damage by gonadotropin-releasing hormone agonist and oral contraceptive in rat model
下载PDF
导出
摘要 目的:探讨促性腺激素释放激素激动剂(GnRHa)和口服避孕药(OC,达英-35)对注射环磷酰胺(CTX)大鼠卵巢功能的保护作用。方法:实验分为6组:空白对照组、CTX组、OC组、GnRHa组、OC保护组、GnRHa保护组,每组15只,分别接受生理盐水、CTX、达英-35、GnRHa、达英-35+CTX、GnRHa+CTX注射或灌胃。阴道涂片观察大鼠动情周期,以放射免疫法检测血清雌二醇(E2)和卵泡刺激素(FSH)浓度,每组在停药当天、15天及30天分别处死5只大鼠,观察卵巢重量、卵巢结构及各级卵泡数目。结果:停药后30天,OC保护组和GnRHa保护组的E2浓度分别为51.33±2.00pg/ml、44.38±5.98pg/ml,FSH浓度分别为3.69±0.28mIU/ml、3.35±0.22mIU/ml,两组比较及与空白对照组(51.76±2.57pg/ml、3.44±0.20mIU/ml)相比,差异均无统计学意义;与CTX组(21.78±2.11pg/ml、6.24±0.22mIU/ml)比较,差异有统计学意义。OC保护组和GnRHa保护组的卵巢重量、卵泡数量与空白对照组相比,差异无统计学意义,明显高于CTX组,两组间比较差异亦无统计学意义。结论:GnRHa和口服避孕药均能减轻化疗药物对卵巢功能的损伤,从而保护卵巢储备功能。 Objective:To compare the effect of gonadotropin-releasing hormone agonist (GnRHa) and oral contraceptive ( OC, Diane-35 ) against cyclophosphamide (CTX) induced gonadotoxieity in female rats. Methods: The experiment consisted of 6 groups : control group, CTX group, OC group, GnRHa group, OC protective group and GnRHa protective group, re- ceived normal saline, CTX, OC, GnRHa, OC + CTX and GnRHa + CTX respectively. Vaginal smear was used to judge the estrous cycle,the serum estradiol( E2 ) and follicle-stimulating hormone(FSH) concentration was measured by radio-immuno assay, and respectively 5 rats were killed just the day, 15 days and 30 days after stopping medication to compare the weight of the ovary, the nmnbers of the follicle. Results: After 30 days, the serum estradiol in OC protective and GnRHa protective group were 51.33±2.00pg/ml,44.38±5.98pg/ml, the FSH concentra- tion in these groups were 3.69±0.28mIU/ml,3.35±0.22mIU/ml respectively. There was no statistical difference between the two groups, and between the two groups and control group. But there was significant difference between the two groups and CTX group. The ovarian weight and follicle numbers of OC protective and GnRHa protective group were similar to those of control group, but higher than those of CTX group. And there was no significant difference between the two groups. Conclusion:GnRHa and oral conceptive can both decrease the CTX-induced damage to the ovarian function, and protect the ovarian reserve function.
出处 《现代妇产科进展》 CSCD 北大核心 2011年第4期296-299,共4页 Progress in Obstetrics and Gynecology
基金 广东省医学科研基金(No:B2010203)
关键词 促性腺激素释放激素激动剂 口服避孕药 化疗 卵巢损伤 Gonadotropin-releasing hormone agonist Oral contraceptive Chemothera-py Ovarian damage
  • 相关文献

参考文献9

  • 1付霞霏,何援利.化疗所致卵巢早衰动物模型的建立[J].广东医学,2008,29(12):1952-1954. 被引量:47
  • 2Devine PJ, Sipes IG, Hoyer PB. Initiation of delayed ovoritoxicity by in vitro and in vivo exposures of rat ovaries to 4-vinylcyclohexeneiepoxide [J]. Reprod Toxicol, 2004, 19 (Pt 1):71-77.
  • 3Rebar RW. Premature ovarian failure [J]. Obstet Gynecol ,2009,113 (6) : 1355-1363.
  • 4Knobf MT. The influence of endocrine effects of adjuvant therapy on quality of life out comes in younger breast cancer survivors[J]. Oncol,2006,11 (2) :96-110.
  • 5Ataya KM, McKanna JA, Weintraub AM, et al. A luteinizing hormone-releasing hormone agonist for the prevention of chemotherapy-induced ovarian follicular loss in rats [J]. Cancer Res, 1985,45 ( 8 ) :3651-3656.
  • 6Blumenfeld Z, Eckman A. Preservation of fertility and ovarian function and minimization of chemotherapy-induced gonadotoxicity in young women by GnRH-a [J]. J Natl Cancer Inst Monogr,2005,34(3 ) :40-43.
  • 7Waxman JH,Ahmed R, Smith D, et al. Failure to preserve fertility in patients with Hodgkin's disease [J]. Cancer Chemother Pharmacol, 1987,19 ( 2 ) : 159-162.
  • 8Letterie GS. Anovulation in the prevention of cytotoxic-induced follicular attrition and ovarian failure[J]. Hum Reprod,2004,19 (4).831-837.
  • 9曹泽毅.甾体激素避孕药[M].北京:中华妇产科学,1999:2431-2509.

二级参考文献8

  • 1MESKHI A, SElF M W. Premature ovarian failure[J]. Curr Opin Obstet Gynecol, 2006, 18 (4) : 418 - 426.
  • 2DEVINE P J, SIPES I G, HOYER P B. Initiation of delayed ovotoxicity by in vitro and in vivo exposures of rat ovaries to 4 - vinylcyclohexene diepoxide[J]. Repro Toxicol, 2004, 19(1 ) : 71 -77.
  • 3DESMEULES P, DEVINE P J. Characterizing the ovotoxicity of cyclophosphamide metabolites on cultured mouse ovaries[ J ]. Toxicol Sci, 2006, 90(2) : 500 -509.
  • 4MOLINA J R, BARTON D L, LOPRINZI C L. Chemotherapy - induced ovarian failure: manifestations and management [ J ]. Drug Saf, 2005, 28(5) : 401 -416.
  • 5MASSIN N, GOUGEON A, MEDURI G, et al. Significance of ovarian histology in the management of patients presenting a premature ovarian failure[J].Hum Reprod, 2004, 19(11 ) : 2 555 - 2 260.
  • 6DAVIS B J, HEINDEL J J. Ovarian toxicants: multiple mechanisms of action[ M]//KORACH K S. Reproductive and developmental toxicology. New York : Dekker, 1998 : 373 - 395.
  • 7GREENWALD G S, ROY S K. Follicular development and its control[ M]//KNOBIL E, NEILL J . The physiology of reproduction. New York : Raven Press, 1994 : 629 - 724.
  • 8LOPEZ S G, LUDERER U. Effects of cyclophosphamide and buthionine sulfoximine on ovarian glutathione and apoptosis[J]. Free Radic Biol Med, 2004, 36(11) : 1 366 -1 377.

共引文献47

同被引文献92

引证文献8

二级引证文献14

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部