排序方式: 共有16条查询结果,搜索用时 15 毫秒
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采用乳过氧化物酶-葡萄糖氧化酶法放射性碘标记国产GnRH激动剂D-色~6-GnRH,用阴离子交换柱层析分离纯化,自身置换曲线计算出标记物比活性为700~1000μCi/μg。~(125)Ⅰ-D-色~6-GnRH与大鼠卵巢细胞膜有特异性结合,结合不受P物质、胰高糖素、生长素释放抑制素、促甲状腺素释放激素、血管紧张素Ⅱ等的竞争抑制。~(125)ⅠD-色~6-GnRH与肾皮质、骨骼肌、心肌等没有特异性结合,与大鼠胎盘有部分结合。大鼠卵巢GnRH受体与垂体GnRH受体的亲和常数基本相同,Ka2.43×10~9M~(-1);结合位点为垂体的20%左右,46.06fm/mg蛋白。本实验表明大鼠卵巢存在着特异性的GnRH受体,有助于阐明GnRH及其类似物的垂体外作用机理。 相似文献
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前列腺素和γ干扰素对人黄体细胞甾体激素生成的影响及相互作用 总被引:4,自引:0,他引:4
我们以前的工作显示T-淋巴细胞产生的细胞因子γ干扰素(IFN-γ),可能在人黄体退化的过程中,通过抑制黄体孕酮生成而起作用。已知在大多数哺乳类动物中,前列腺素F2a(PGF2a)是一个重要的溶黄体因子。本工作对γ干扰素与前列腺素的关系作了进一步探讨。实验将人黄体细胞置于有或无γ干扰素的条件下培养4天,同时,测定孕酮、PGF2a、PGE2和6-酮-PGF1a的生成。伴随着γ干扰素对孕酮合成的抑制,观察到一个前列腺素合成的双相模式反应。即暴露于γ干扰素24h后,PGF2a和PGF1a的合成轻微降低,而培养96h后PGE2的合成增加。在另一实验中,发现PGE2和PGF2a对不同期的人黄体细胞在培养48h和96h后均有促黄体作用。此外,在消炎痛显著抑制PG合成的同时,γ干扰素仍能同样抑制其黄体细胞产生孕酮。这些结果提示:观察到γ干扰素引起的抑制孕酮产生似乎并非由前列腺素造成的,因为在同时加入可以抑制前列腺素合成的消炎痛时,这种抑制效果并不受影响。 相似文献
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本文对19例12~20岁的青少年型血吸虫病性侏儒症患者的LRH和TRH下丘脑-垂体-靶腺轴兴奋试验的检测结果进行了观察。初步表明:该类患者的下丘脑-垂体-靶腺轴反馈机制大致正常。垂体GH、LH、TSH、PRL等激素并不缺乏,其储备功能亦大致正常。但周围靶腺激素不正常,这与垂体性侏儒症等明显不同,亦与中老年晚血患者的情况不同。因此,我们认为使用LRH和TRH作垂体兴奋试验将有利于本病的诊断和鉴别诊断,并有可能把该症从继发性垂体性侏儒症和晚血的分类中区分出来,这对改善其预后也不无裨益。 相似文献
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采用多种实验动物观察表明LHRH类似物丙氨瑞林(1)对下丘脑-垂体-性腺轴具有正向和异向作用,二者与给药剂量、持续时间有关。低剂量1单次或短期给药可诱发兔排卵、大鼠血清促性腺激素LH水平升高、成年雌猴血清雌二醇水平增高、幼小白鼠子宫重量增加。后者与1长期给药使雌性大鼠子宫组织萎缩的作用恰好相反。1长期给药也使大鼠单侧卵巢切除诱发的对侧卵巢代偿性肥大反应受抑。成年雌猴连续给药11个月,诱导血清雌二醇和孕酮升高的反应均较首次注射时的诱导作用为低。 相似文献
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GnRH激动剂对大鼠卵巢GnRH受体的作用 总被引:1,自引:1,他引:0
D-丙~6-去甘~(10)GnRH乙基酰胺(GnRH-A)150μg/天能使正常大鼠卵巢GnRH受体含量增加;去垂体大鼠GnRH-A 15μg/天能使卵巢GnRH受体量增加,加用孕马血清75IU/天后,卵巢GnRH受体又显著减少,血中雌二醇、孕酮增加;在妊娠15天大鼠,GnRH-A 15μg/天同样引起卵巢GnRH受体增加,而血中雌二醇、孕酮则减少,胚胎死亡。GnRH-A对卵巢GnRH受体亲和常数没有影响。本实验结果提示,大剂量GnRH-A对大鼠卵巢GnRH受体有自身诱导作用,促性腺激素使卵巢GnRH受体降调节,GnRH-A终止15天龄大鼠妊娠的作用与卵巢GnRH受体含量增加有关,卵巢GnRH受体含量与血中雌二醇、孕酮水平呈负相关。 相似文献
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Effects and Interactions of Prostaglandins and Interferon-γ on Steroidogenesis of Human Luteal Cells
Previous work from our laboratory has demonstrated that T lymphocyte-derived cytokine, interferon-gamma (IFN-γ) may play a role in human luteal regression by inhibiting luteal progesterone production. Prostaglandin F2a has been known as an important luteolytic factor in a wide range of mammalian species. It was of interest to investigate the effects of IFN-γ on prostaglandin synthesis and their possible interaction with the inhibition on human luteal steroidogenesis. Human luteal cells were cultured for four days in the presence or absence of IFN-γ. Simultaneously, the productions of progesterone, prostaglandin F2a ( PGF2a ), prostaglandin E2 ( PGE2 ), and 6-ketoprostaglandin F1a(PGF1a) were evaluated. Concomitant with the inhibition of progesterone production induced by IFN-γ, a biphasic pattern of response of. prostaglandin synthesis was observed, i.e. a slight decrease of PGF2a and PGF1a after a 48 h exposure to IFN-γ while an increase of PGE2 after 96 h. In a separate experiment, a luteotropic action of PGE2 and PGF2a on human luteal cells from different stages was observed during 48 and 96 h periods of culture. In addition, while indomethacin (INDO) treatment markedly blocked the prostaglandin synthesis, the basal as well as hCG stimulated progesterone production was still inhibited by IFN-γ as usual. These results suggested that prostaglandins appeared to be not responsible for the observed inhibition of progesterone production since the inhibitory effect was not influenced by concurrent treatment with INDO which suppressed prostaglandin synthesis, 相似文献