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环磷酰胺对成年大鼠卵巢的损伤以及GnRHR在卵巢的表达 被引量:14

Cyclophosphamide-induced rat ovarian damage and expression of gonadotropin-releasing hormone receptor in the damaged ovaries
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摘要 目的探讨化疗药物对卵巢的损伤及其可能机制。方法将成年SD大鼠分为2组:生理盐水组和环磷酰胺组。大鼠腹腔注射环磷酰胺;8周后固定一侧卵巢,连续切片,观察卵巢形态学改变并计数卵泡数目;免疫组化法检测GnRHR在卵巢的表达。RT-PCR法检测对侧卵巢GnRHR mRNA的表达。结果环磷酰胺可引起卵巢皮质区原始卵泡发生大量丢失,卵巢间质严重损害,血管发生特征性病理改变;局部发生纤维化。GnRHR mRNA和蛋白质可表达于大鼠卵巢。与对照组相比,环磷酰胺组颗粒细胞GnRHR蛋白表达减少;化疗组GnRHR mRNA表达量低于对照组(P<0.05)。结论GnRHR在化疗卵巢较低水平的表达,提示化疗晚期卵巢局部微环境的紊乱。 Objective To investigate ovarian follicular damage induced by chemotherapeutic agents and gonadotropin- releasing hormone receptor (GnRHR) expression in the damaged ovaries in rats. Methods Two groups of adult SD rats were subjected to intraperitoneal injection of a single-dose cyclophosphamide and saline, respectively, and 8 weeks later, the ovaries were taken for observing the ovarian damages. The distribution of GnRHR was detected with immunohistochemistry, and RT-PCR was used to determine the expression of GnRHR mRNA in the rat ovaries. Results Massive primordial follicular loss occurred in the ovaries of rats exposed to cyclophosphamide with also evident stromal ovarian blood vessel damages and focal fibrosis. Both the protein and mRNA expressions of GnRHR were detected in normal rat ovaries, but in rats exposed to cyclophosphamide, the expressions were significantly lowered in the ovaries (P〈0.05). Conclusion Low-level GnRHR expressions in the ovaries of rats with cyclophosphamide exposure suggest microenvironment disturbances in the damaged rat ovaries in advanced stage of chemotherapy.
出处 《南方医科大学学报》 CAS CSCD 北大核心 2007年第11期1714-1717,共4页 Journal of Southern Medical University
基金 卫生部部属(管)医疗机构临床学科重点项目 国家教育部博士点基金(20050558093) 中国博士后基金(20060390755)~~
关键词 环磷酰胺 卵巢 GnRHR 免疫组化 RT-PCR cyclophosphamide ovary GnRHR immunohistochemistry reverse transcription-polymerase chain reaction
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  • 1Meirow D, SchiffE. Appraisal of chemotherapy effects on reproductive outcome according to animal studies and clinical data[J]. J Natl Cancer Inst Monogr, 2005, 34: 21-5.
  • 2Yoshino O, Osuga Y, Koga K, et al. Upregulation ofinterleukin-8 by hypoxia in human ovaries[J]. Am J Reprod Immunol, 2003, 50(4): 286-90.
  • 3Choi JH, Gilks CB, Auersperg N, et al. Immunolocalization of gonadotropin-releasing hormone (CmRH)-I, GnRH-II, and type I CmRH receptor during follicular development in the human ovary [J]. J Clin Endocrinol Metab, 2006, 91(11): 4562-70.
  • 4Cohen DP, Stein EM, Li Z, et al. Molecular analysis of the gonadotropin-releasing hormone receptor in patients with polycystic ovary syndrome[J]. Fertil Steril, 1999, 72(2): 360-3.
  • 5Flaws JA, Doerr JK, Sipes IG, et al. Destruction ofpreantral follicles in adult rats by 4-vinyl- 1-cyclohexene diepoxide [ J]. Reprod Toxicol, 1994, 8(6): 509-14.
  • 6Whitelaw PF, Eidne KA, Sellar R, et al. Gonadotropin-releasing hormone receptor messenger ribonucleic acid expression in rat ovary [J]. Endocrinology, 1995, 136(1): 172-9.
  • 7Cheng CK, Leung PC. Molecular biology of gonadotropin-releasing hormone (GnRH)-I, GnRH-II, and their receptors in humans [J]. Endocr Rev, 2005, 26(2): 283-306.
  • 8Wong WY, Richards JS. Induction ofprostaglandin H synthase in rat preovulatory follicles by gonadotropin-releasing hormone [J]. Endocrinology, 1992, 30(6): 3512-21.
  • 9Natraj U, Richards JS. Hormonal regulation, localization, and functional activity of the progesterone receptor in granulosa cells of rat preovulatory follicles [ J ]. Endocrinology, 1993, 133(2): 761-9.

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