【目的】 应用兴奋性氨基酸受体激动剂建立雌性大鼠性早熟模型。 【方法】 雌性SD大鼠50只,随机分为5组:实验Ⅰ组(性早熟青春早期组),实验Ⅱ组(性早熟青春中期组),对照Ⅰ组(正常青春前期组),对照Ⅱ组(正常青春早期组),对照Ⅲ组(正常青春中期组),实验组皮下注射N-甲基-D,L-天冬氨酸(NMA),对照组注射生理盐水,观察大鼠阴道开放时间及性周期,测量子宫指数、卵巢指数、卵巢黄体出现率、子宫壁厚度、黄体生成素浓度。 【结果】 实验组大鼠阴道开放及首次发情间期出现的时间较对照组提前,实验组各项指标较对照Ⅰ组有显著差异,实验Ⅰ组较对照Ⅱ组、实验Ⅱ组较对照Ⅲ组差异无统计学意义。 【结论】 应用兴奋性氨基酸受体激动剂可以使雌性大鼠正常的性发育提前,建立性早熟模型。
Abstract
【Objective】 Establish the precocious puberty model in female rats induced by excitatory amino acids receptor agonist. 【Methods】 Fifty 26-day-old female rats were randomly assigned to 5 groups, experimental groupⅠ(early phase of precocious puberty), the second experimental groupⅡ(metaphase of precocious puberty), control groupⅠ(normal prepuberty), control groupⅡ(early phase of normal puberty), control groupⅢ(metaphase of normal puberty). Study group received subcutaneous injection of N-methyl-DL-aspartate acid(NMA) twice a day until vaginal opening(VO) occurred and control groups received saline. The parameters of puberty were analyzed, which including index of ovary, index of uterus, incidence of corpora lutea, thickness of uterus and serum luteinizing hormone. 【Results】 The age of VO and first diestrus of experimental groups were earlier than the control groups. The parameters of puberty in experimental groups were different from control groupⅠ. The parameters of puberty in experimental groupⅠ were not different from control groupⅡ. The parameters of puberty in experimental groupⅡ were not different from control groupⅢ. 【Conclusions】 The precocious puberty model in female rats were successfully established by subcutaneous injection of NMA.
关键词
青春期 /
性早熟 /
兴奋性氨基酸 /
N-甲基-D /
L-天冬氨酸
Key words
puberty /
precocious puberty /
excitatory amino acids /
N-methyl-DL-aspartate acid
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参考文献
[1] Plant TM. The role of Kiss-1 in the regulation of puberty in higher primates[J]. Eur J Endocrinol,2006,155:11-16.
[2] Plant TM, Barker-Gibb ML. Neurobiological mechanisms of puberty in higher primates[J]. Hum Reprod Update,2004,10(1):67-77.
[3] Carbone S, Szwarcfarb B, Reynoso R, et al. Leptin stimulates LH secretion in peripubertal male rats through NMDA receptors[J]. EndocrRes,2005,31(4):387-396.
[4] Plant TM, Ramaswamy S, Dipietro MJ. Repetitive activation of hypothalamic G protein- coupled receptor 54 with intravenous pulses of kisspeptin in the juvenile monkey (Macaca mulatta) elicits a sustained train of gonadotropin- releasing hormone discharges[J]. Endocrinology,147(2):1007-1013.
[5] Terasawa E, Fernandez DL. Neurobiological mechanisms of the onset of puberty in primates[J]. Endocr Rev,2001,22(1):111-151.
[6] Clarkson J, Han SK, Liu X, et al. Neurobiological mechanisms underlying kisspeptin activation of gonadotropin-releasing hormone(GnRH) neurons at puberty[J]. Mol Cell Endocrinol,2010,324(1-2):45-50.
[7] Moguilevsky JA, Wuttke W. Changes in the control of gonadotrophin secretion by neuro- transmitters during sexual development in rats[J]. Exp Clin Endocrinol Diabetes,2001,109(4):188-195.
[8] Nyberg CL, Hiney JK, Minks JB, et al. Ethanol alters N-methyl-DL-aspartic acid-induced secretion of luteinizing hormone releasing hormone and the onset of puberty in the female rat[J]. Neuroendocrinology,1993,57(5):863-868.
[9] 田占庄,赵宏,陈伯英.达那唑诱导的雌性性早熟大鼠GnRH及其受体mRNA的表达[J].中华内分泌代谢杂志,2003,19(5):399-401.
[10] Morishita H, Takemoto M, Kondo H, et al. Induction of true precocious puberty by neonatal treatment with danazol in female rats[J]. Neurosci Lett,1993,157(1):33-36.
[11] Honaramooz A, Chandolia RK, Beard AP, et al. Excitatory amino acid regulation of gonadotropin secretion in prepubertal heifer calves[J]. Biol Reprod,1998,59(5):1124-1130.