GnRH-a体外对人卵巢黄素化颗粒细胞雌二醇和孕酮分泌量的影响

目的 :观察促性腺素释放激素激动剂 (GnRH -a)在体外对人卵巢黄素化颗粒细胞雌二醇 (E2 )和孕酮 (P)分泌量的影响。方法 :培养人卵巢黄素化颗粒细胞 ,分别用终浓度为 1.0、10 .0、10 0 .0ng ml的GnRH -a刺激 ,同时设对照组 ,培养时间为 2、4、6d。用放射免疫法检测黄素化颗粒细胞E2 和P的分泌量。结果 :培养 2d ,GnRH -a中、高浓度组E2 和P分泌量分别为 (12 2± 37) %、(12 8± 2 4 ) % ;(143± 32 ) %、(137± 2 9) %对照组为10 0 % ,均显著高于对照组 (P <0 .0 5) ;低浓度组E2 和P分泌量与对照组差异无显著性。随着细胞培养天数的增加 ,GnRH -a中、高浓度组E2 分泌量明显低于对照组 ,高浓度组E2 分泌量与培养天数呈负相关 (r =- 0 .75,P <0 .0 5)。结论 :GnRH -a对黄素化颗粒细胞分泌甾体激素功能的影响随着作用时间和浓度的不同而变化     

子宫内膜间质细胞体外蜕膜化的激素调节

目的 探讨甾体激素、黄体生成素释放激素（LHRH）、人绒毛膜促性腺激素（hCG）、促卵泡激素（FSH）在子宫内膜间质细胞蜕膜化过程中的作用。方法 取18例育龄期妇女的增殖期子宫内膜,行体外分离、培养其间质细胞,加入生理剂量的雌二醇（E2）、孕酮(P)、睾酮（T）,以及LHRH、hCG、FSH,在相差显微镜下观察细胞的形态学改变,采用放射免疫法测定培养液中泌乳素（PRL）的含量。结果 E2、P、T对子宫内膜间质细胞的生长及分化均有调节作用,RPL开始上升与多角形细胞出现的时间相一致,P、T对子宫内膜膜间质细胞蜕膜化、分泌PRL起主要作用（P＜0.01）,P与E2、T有协同作用。LHRH hCG、FSH对子宫内膜间质细胞蜕膜化、分泌PRL均有促进作用（P＜0.01）,以hCG的作用最强。结论 P、T、E2在子宫内膜间质细胞生长分化过程中起重要作用,LHRH、hCG、FSH直接作用于子宫内膜本身而参与蜕膜化的调节。     

白介素-6调节颗粒细胞雌孕激素分泌的作用

目的 :探讨白介素 -6 (IL -6 )对颗粒细胞分泌雌孕激素的影响。方法 :收集行 IVF-ET穿卵时的颗粒细胞作体外培养 ,在有或无 FSH条件下 ,以不同浓度的 rh IL-6作用于颗粒细胞 ,2 4、48、72和 96 h后收集培养液作雌二醇、孕酮测定 ,观察基因重组人白介素 -6 (rh IL-6 )对体外培养中的颗粒细胞分泌雌二醇、孕酮的影响 ;通过 m RNA狭缝杂交 (m RNA slotblot)检测颗粒细胞是否存在 IL-6 R m RNA。结果 :在无 FSH条件下 ,rh IL-6对颗粒细胞分泌雌二醇有抑制作用 ,对孕酮分泌的影响不明显 ;而加入 FSH后 ,发现 rh IL-6对 FSH刺激颗粒细胞所分泌的雌二醇、孕酮均有明显抑制作用。这些作用呈现一定的时间和剂量依赖性。结论 :rh IL-6可抑制 FSH刺激颗粒细胞所致的甾体激素分泌 ,从而参与调节卵巢功能。     

甾体激素对绒毛外滋养细胞表达HLA-G蛋白的影响

目的:探讨甾体激素(E_2、P_4)对绒毛外滋养细胞表达HLA-G的影响。方法:将分离培养的绒毛外滋养细胞(EVT)分成E_2组、孕酮(P_4)组、E_2+P_4组和空白对照组,分别向各组EVT培养液中加入不同浓度的17β-雌二醇、孕酮及17β-雌二醇+孕酮,空白对照组则不加任何激素,48h后,流式细胞仪检测各组HLA-G蛋白的表达。结果:①单独使用E_2或P_4均能上调EVT表达HLA- G蛋白,上调作用与其浓度关系密切,与对照组相比,差异有显著性(P＜0．01);②联合应用E_2+P_4亦上调EVT表达HLA-G蛋白,1000 nmol/L的E_2+P_4组HLA-G蛋白的表达,明显高于低浓度组(1nmol/L、10nmol/L、100nmol/L),差异有显著性(P＜0．01);③低浓度的E_2+P_4组(1nmol/L)HLA- G蛋白的表达高于同浓度的P_4组(P＜0．05),而低于同浓度的E_2组(P＜0．001);1000nmol/L,E_2+P_4组HLA-G表达显著高于单纯的E_2、P_4组(P＜0．01)。结论:①低浓度的E_2、P_4对HLA-G调节呈拮抗作用,高浓度E_2和P_4则以协同作用调节HLA-G的表达;②HLA-G可能参与了卵巢甾体激素调节胚胎植入进程。     

雌、孕激素对人早孕蜕膜基质细胞中B淋巴细胞激活因子受体(BAFFR)表达的影响

目的:初步探讨B淋巴细胞激活因子受体(Bcells-activating factor receptor,BAFFR)在胚胎植入调控中的作用。方法:选取正常早孕妇女人工流产蜕膜组织,分离、提纯早孕蜕膜基质细胞(decidual stromal cells,DSC),培养于含10%去激素胎牛血清培养基内,分为雌二醇(E2)组、孕酮(P4)组、E2+P4组和空白对照(C)组,培养96h。MTT检测细胞的增殖能力;Real-time PCR检测BAFFR mRNA;流式细胞仪检测BAFFR蛋白表达。结果:与C组比较,各实验组DSC增殖能力及BAFFR mRNA水平均无明显变化(P>0.05);BAFFR蛋白定位于DSC胞内,且E2+P4可显著上调其表达(P<0.05)。结论:正常人早孕DSC表达高水平的BAFFR,雌、孕激素联合对其有显著的上调作用,提示BAFFR可能参与胚胎植入的调控及早孕期母-胎界面的免疫调节。     

醋酸棉酚对大鼠成熟卵泡的颗粒细胞产生雌二醇及孕酮功能影响的离体观察

给30天幼龄大鼠皮下注射12IU 孕马血清,48小时后采集发育成熟的卵泡颗粒细胞进行离体培养,并在培养基中加入不同浓度的醋酸棉酚,以观察醋酸棉酚对卵巢甾体激素合成功能的影响。结果发现,棉酚对颗粒细胞分泌孕酮的能力以及对hCG 促进颗粒细胞生成孕酮的能力均有抑制作用。这种抑制作用随棉酚剂量的增加及作用时间的延长而增强。但同样剂量的棉酚对颗粒细胞利用睾酮转化为雌二醇的能力无明显抑制作用。这提示棉酚对颗粒细胞内孕酮生物合成系统有直接抑制作用,而对芳香化酶的活性似无明显干扰作用,表明棉酚对卵巢内甾体激素合成功能的抑制具有选择性。此外,本实验还发现,hCG 的作用在未被完全阻断时,能不同程度地削弱棉酚对颗粒细胞分泌孕酮功能的抑制作用。     

雌孕激素对体外卵泡黄素化颗粒细胞分泌巨噬细胞集落刺激因子的影响

目的　探讨雌、孕激素对卵泡黄素化颗粒细胞 (颗粒细胞 )分泌巨噬细胞集落刺激因子(M CSF)的调节作用。方法　抽取接受卵母细胞单精子显微注射 (ICSI)的 12例妇女的颗粒细胞 ,在不同浓度 ( 0、1× 10 - 7、1× 10 - 6 、1× 10 - 5 、1× 10 - 4、1× 10 - 3 mol L)的雌二醇或孕酮作用下培养 72h ,采用酶联免疫吸附法测定颗粒细胞培养液中的M CSF含量。结果　颗粒细胞在雌二醇或孕酮为 0mol L(即无雌二醇或孕酮作用———基础状态 )的情况下培养 72h后 ,分泌一定量的雌二醇 [( 1 0 2± 0 2 3 )×10 - 7mol L]、孕酮 [( 1 0 0± 0 12 )× 10 - 5 mol L]和少量的M CSF[( 4 7± 15)ng L] ;在 1× 10 - 6 ～ 1× 10 - 3mol L浓度的雌二醇作用下 ,M CSF分泌增加 ,其分泌随雌二醇浓度的增加而增加 ,较基础状态分别增加 2 3、4 5、6 9和 7 9倍 ;在≥ 1× 10 - 6 mol L各浓度的雌二醇作用下 ,M CSF分泌与基础状态比较 ,差异均有显著性 (P均 <0 0 5) ;在 1× 10 - 7mol L浓度的雌二醇作用下 ,M CSF分泌与基础状态比较 ,差异无显著性 (P >0 0 5) ;在 1× 10 - 7～ 1× 10 - 3 mol L浓度的孕酮作用下 ,M CSF分泌与基础状态比较 ,差异均无显著性 (P >0 0 5)。结论　雌二醇能促进颗粒细胞M CSF的分泌 ,孕酮对颗     

核苷酸还原酶小亚基反义寡核苷酸对人绒毛膜癌细胞体外生长的影响

目的　探讨核苷酸还原酶小亚基 (RRM2 )反义寡核苷酸 (ASODN)对人绒毛膜癌细胞株JAR细胞体外生长的影响。方法　以脂质体为载体 ,将人工合成的分别位于RRM2mRNA核苷酸序列第 6 2 6～ 6 4 5 (编码区 )和第 15 72～ 15 91(3′端非编码区 )位点且全程硫代修饰的两条ASODN片断 (前者称ASODN1,后者称ASODN2 )导入JAR细胞中 ,用四甲基偶氮唑蓝 (MTT)比色法检测细胞存活率 ,免疫印迹法和RT PCR技术检测ASODN对RRM2蛋白和mRNA表达的影响。结果　 (1)ASODN1对JAR细胞的抑制作用呈剂量和时间效应 :10 0nmol/LASODN1作用后JAR细胞的生长抑制率为 (8 10±1 18) % ;随着ASODN1浓度的增加细胞生长抑制作用增强 ,ASODN1浓度为 4 0 0nmol/L时其细胞生长抑制率为 (2 7 70± 3 6 8) % ,与ASODN1浓度为 0时 [(0 16± 0 12 ) % ]比较 ,差异有极显著性 (P =0 0 0 0 )。 2 0 0nmol/LASODN1作用 2 4h后 ,细胞生长抑制率为 (13 98± 1 4 5 ) % ;4 8h[为 (18 90±4 85 ) % ]达到高峰 ,72h抑制作用 [为 (19 5 3± 5 0 0 ) % ]不再明显增强 ,分别与作用时间为 0时 [(0 16± 0 31) % ]比较 ,差异均有极显著性 (P =0 0 0 0 )。 (2 )JAR细胞RRM2蛋白和mRNA的表达 :2 0 0nmol/LASODN1作用 12h ,RRM2蛋白和mRNA表达水平开始下降     

人滋养叶细胞各种肽类激素的受体动态

胎盘滋养叶组织分泌两大类激素,其一是雌三醇(E_3)和孕酮等类固醇激素;其二是肽类激素,这些激素是由合体滋养叶细胞产生,对妊娠的维持、胎儿发育具有重要作用。虽然有人报告,人滋养叶细胞存在着胰岛素、雌激素、雄激素和转铁蛋白的各种受体,但有关其他激素受体存在的报告几乎没有。因此本文就滋养叶细胞分泌的人绒毛膜促性腺激素(hCG)、人胎盘泌乳素(hPL)的受体和滋养叶细胞本身虽不分泌但在其中存在的肾上腺     

电压门控钾离子通道对卵巢黄素化颗粒细胞增殖、分泌及凋亡的影响

目的 探讨电压门控钾离子通道(Kv)对人绒毛膜促件腺激素(hCG)诱导的卵巢黄素化颗粒细胞增殖、分泌及凋亡的影响.方法 收集2007年11月至2008年2月行体外受精-胚胎移植患者的卵泡液共25份,密度梯度法获得卵巢黄素化颗粒细胞,采用RT-PCR技术检测颗粒细胞中KvmRNA的表达.将培养贴壁后的颗粒细胞按干预方式分为空白组、4氨基吡啶(4-AP)组、hCG组和hCG+4-AP组共4组,hCG和4-AP的终浓度分别为1250 U/L、5 nmol/L.培养24 h后,采用化学发光法测定各组孕酮水平;采用流式细胞仪和分光光度法检测各组颗粒细胞的凋亡情况;采用四甲基偶氮唑监(MTT)比色法检测各组颗粒细胞的增殖、抑制情况.结果 (1)培养24 h后,空白组、4-AP组、hCG组和hCG+4.AP组颗粒细胞中的孕酮水平分别为(547 ±64)、(206 ±32)、(1991±172)和(763 ±79)nmol/L.4-AP组、hCG组分别与空白组比较,差异均有统计学意义(P<0.01);hCG+4-AP组与hCG组比较,差异也有统计学意义(P<0.01).(2)培养24 h后,4-AP组颗粒细胞抑制率为19.7%,与空白组(0)比较,差异有统计学意义(P<0.05);hCG+-AP组为34.6%,与hCG组(0)比较,差异也有统计学意义(P<0.01).4-AP组、hCG+4-AP组的颗粒细胞增殖率分别为80.3%、68.2%,分别与空白组(100%)比较,差异均有统计学意义(P<0.05、P<0.01);hCG组(100.4%)高于空白组,但差异无统计学意义(P>0.05).(3)培养24 h后颗粒细胞的凋亡率及半胱氨酸天冬氨酸蛋白酶(caspase-3)活性,4-AP组分别为(40±5)%和0.049 ±0.009,均高于空白组[(17±4)%和0.029±0.008],hCG+4-AP组[(25±4)%和0.039±0.008]也均高于hCG组[(15 ±3)%和0.022 ±0.007],差异均有统计学意义(P<0.01).结论 4-AP能够抑制卵巢黄素化颗粒细胞和经hCG诱导的颗粒细胞的孕酮分泌,町能与其抑制增殖、促进凋亡有关.Kv在卵巢黄素化颗粒细胞分泌、增殖及凋亡过程中起重要的作用.     

Progesterone and human placental lactogen inhibit leptin secretion on cultured trophoblast cells from human placentas at term.

The placenta is an important source of leptin production that contributes to the state of hyperleptinemia observed in pregnant women. Moreover, the synthesis of leptin and its receptors by syncytiotrophoblast cells suggests a potential paracrine or autocrine action of leptin in the placenta. In the present study we examined the effect of gestational hormones, human chorionic gonadotropin (hCG), human placental lactogen (hPL), progesterone and estradiol, on in vitro leptin release by human term trophoblast cells in culture. Placentas at term were obtained immediately after delivery from mothers with uncomplicated pregnancies. Leptin levels were measured by enzyme-linked immunosorbent assay in culture media of trophoblasts maintained in monolayer culture for 24, 48 and 72 h with different hormonal treatments or placebo. Treatment with hPL and progesterone led to a time- and dose-dependent decrease in leptin release that was statistically significant after 24 h, with a maximal effect after 72 h of incubation. In contrast, incubation with estradiol and hCG did not have exhibit any effect on leptin secretion at any of the doses and times assayed in this work. The results obtained in this study support that leptin can be considered a gestational hormone implied in the endocrine function of the placenta and that its secretion is at least partially regulated by steroid and peptidic reproductive hormones in trophoblast cells in vitro.     

Progesterone and human placental lactogen inhibit leptin secretion on cultured trophoblast cells from human placentas at term

The placenta is an important source of leptin production that contributes to the state of hyperleptinemia observed in pregnant women. Moreover, the synthesis of leptin and its receptors by syncytiotrophoblast cells suggests a potential paracrine or autocrine action of leptin in the placenta. In the present study we examined the effect of gestational hormones, human chorionic gonadotropin (hCG), human placental lactogen (hPL), progesterone and estradiol, on in vitro leptin release by human term trophoblast cells in culture. Placentas at term were obtained immediately after delivery from mothers with uncomplicated pregnancies. Leptin levels were measured by enzyme-linked immunosorbent assay in culture media of trophoblasts maintained in monolayer culture for 24, 48 and 72?h with different hormonal treatments or placebo. Treatment with hPL and progesterone led to a time- and dose-dependent decrease in leptin release that was statistically significant after 24?h, with a maximal effect after 72?h of incubation. In contrast, incubation with estradiol and hCG did not have exhibit any effect on leptin secretion at any of the doses and times assayed in this work. The results obtained in this study support that leptin can be considered a gestational hormone implied in the endocrine function of the placenta and that its secretion is at least partially regulated by steroid and peptidic reproductive hormones in trophoblast cells in vitro.     

Hickman catheter use in a pregnant patient requiring therapeutic heparin anticoagulation

This study was undertaken to investigate the possible regulatory effects of the sex steroids estradiol and progesterone and the protein hormone human chorionic gonadotropin (hCG) on prolactin (PRL) production by human decidua in vitro. Decidual tissue obtained from chorionic membranes was incubated in serum-free Dulbecco's modified Eagle's medium in the steroid experiments and in media supplemented with 5% fetal calf serum in the hCG experiments. Daily media samples up to 90 hours were assayed for PRL by radioimmunoassay. Estradiol in a final medium concentration of 1 ng/ml significantly stimulated overall PRL production within 48 to 72 hours (n = 26, p = 0.0007). This difference was not, however, significant at 24 hours (p = 0.07). Progesterone alone in final concentrations of 100 ng/ml failed to demonstrate any effect relative to controls (n = 17, p = 0.5). A daily change of media with the addition of fresh progesterone also failed to affect PRL production (n = 8, p = 0.35). The same estradiol and progesterone concentrations, in combination, suppress PRL production over 72 hours, significant at p = 0.0001 (n = 9). When estradiol was administered initially and progesterone was added after 24 hours, the PRL production diminished significantly (n = 9, p = 0.0003). hCG stimulated PRL production in serum-supplemented media only at a dose of 10⁴ mlU/ml (p = 0.0001). Finally, this effect could be delayed for 24 hours (p = 0.0001). We interpret these data to suggest a stimulatory role for estradiol in the synthesis of PRL by human term decidua in vitro and an estradiol-modulated suppressive effect for progesterone—both effects in a manner consistent with their similar effects on pituitary cell cultures. Also, hCG has a definite but poorly understood role in stimulating in vitro decidual PRL production.     

Interleukin-1: local production and modulation of human granulosa luteal cells steroidogenesis.

OBJECTIVES: To investigate the possibility of local interleukin-1 (IL-1) and IL-1 inhibitor production by human granulosa and cumulus cells and to assess their direct effects on the steroidogenesis of these cells in vitro. DESIGN: Prospective study. PARTICIPANTS: Normal ovulatory women undergoing ovulation induction for in vitro fertilization. INTERVENTION: Pretreatment of patients with gonadotropin-releasing hormone analogue, human menopausal gonadotropin, and human chorionic gonadotropin (hCG). MAIN OUTCOME MEASURES: Retrieval and isolation of granulosa luteal cells and follicular fluid (FF). Granulosa luteal cells and cumulus cells cultured and analyzed by fluorescent activated cell sorter. Follicular fluid separated and bioassayed for IL-1 and IL-1 inhibitory activity. Steroid measurement performed. Interleukin-1 inhibitor purified. Interleukin-1 and IL-1 inhibitor bioassay performed. Statistical analysis made and interpreted. RESULTS: Interleukin-1, but not IL-1 specific inhibitory activity, was found in granulosa and cumulus cell cultures and also in FF, only after its purification on a high-pressure liquid chromatography column. Under nonstimulated conditions, neither IL-1 nor IL-1 inhibitor had any effect on basal progesterone (P) or estradiol (E2) secretion. However, IL-1 inhibitor demonstrated significant (P < 0.01) inhibition of hCG-stimulated P secretion (from 200 to 110 ng/10,000 cells per 24 hours). In addition, IL-1 demonstrated a significant (P < 0.05) and dose-dependent inhibition of hCG-stimulated E2 production (from 6,832 +/- 460 to 4,237 +/- 141 pg/10,000 cells per 24 hours). CONCLUSIONS: Interleukin-1 may exert a significant local autocrine regulatory role in the human ovary.     

米非司酮对人绒毛膜癌细胞株体外作用的观察

目的 探讨米非司酮对人绒毛膜癌细胞株ＪＡＲ的作用。方法 采用四甲基偶氮唑蓝（ＭＴＴ）比色法,观察１、５、１０、２０μｍｏｌ／Ｌ的米非司酮对ＪＡＲ细胞的杀伤活性,通过免疫组化及酶联免疫法（ＥＬＩＳＡ）检测用药后,ＪＡＲ细胞均有杀伤作用,并呈剂量依赖性,以２０μｍｏｌ／Ｌ浓度的米非司酮作用最强,杀伤率达７３．１９％。５μｍｏｌ／Ｌ的米非司酮与ＪＡＲ细胞作用７２小时,Ｋｉ－６７抗原阳性率明显下降,第３天     

Effect of leptin on the regulation of placental hormone secretion in cultured human placental cells.

Placenta is an important source of leptin during pregnancy that contributes to the high plasma leptin levels in pregnant women. Leptin and its functional receptors are synthesized in trophoblast cells that, in turn, secrete gestational hormones supporting a paracrine or autocrine role for leptin in the endocrine activity of the placenta. In the present study we examined the effect of leptin on in vitro release of gestational hormones (human chorionic gonadotropin (hCG), human placental lactogen (hPL), progesterone, estrogens and testosterone) by human term placental cells in culture. Placentas at term were obtained immediately after delivery from mothers with uncomplicated pregnancies. Progesterone, hCG, hPL, estradiol, estrone, estriol and testosterone levels were measured by different assays in culture media of cells maintained in monolayer culture after incubation for 12, 24, 48 or 72 h with leptin or placebo. Incubation with leptin did not modify hCG, hPL, progesterone, estriol and estrone secretion for any of the doses and times assayed. However, leptin led to a dose-dependent decrease in estradiol release. This effect was observed when treatment with recombinant human leptin spanned from 12 to 72 h. At this time an increase in testosterone levels was observed in leptin-treated cells versus placebo. These results indicate that leptin can be considered a gestational hormone implied in the endocrine function of the placenta, with an important role in control of the production of steroid reproductive hormones in placental cells in vitro.     

Effects of human chorionic gonadotropin,estradiol, and progesterone on interleukin-18 expression in human decidual tissues

Interleukin (IL)-18 is a proinflammatory cytokine which mediates a myriad of inflammatory responses during pregnancy. Changes in IL-18 levels have been linked to complications during pregnancy. This study was designed to assess the effects of estradiol, human chorionic gonadotropin (hCG), and progesterone on IL-18 expression in human decidual tissues. Uterine deciduas from women with normal pregnancy, spontaneous abortion, and progesterone treated spontaneous abortion were collected, and the effects of hormones on the viability of decidual cells and IL-18 secretion were detected by MTT and ELISA assays. We found that Estradiol, hCG, and progesterone inhibited decidual cell growth independent of dosage and time.IL-18 secretion in the spontaneous abortion group was increased in the decidual cells over time, but all hormones significantly reduced its secretion (p?相似文献   

Steroidogenesis of cultured granulosa cells in women at risk for ovarian hyperstimulation syndrome.

OBJECTIVE: To determine if cultured human granulosa cells (GCs) obtained from women at risk for ovarian hyperstimulation syndrome (OHSS) possess altered steroidogenic capacity. DESIGN: Prospective analysis of 28 consecutive in vitro fertilization-gamete intrafallopian transfer (IVF-GIFT) cycles. SETTING: In Vitro Fertilization Program at Rush Presbyterian St. Luke's Medical Center in Chicago, Illinois. PATIENTS: Eighteen patients (group I) with serum estradiol (E2) levels > 7,342 pmol/L on the day of exogenous human chorionic gonadotropin (hCG) administration (day 0) with > 10 ovarian follicles present (high risk for OHSS); 10 patients (group II) with E2 < or = 7,342 pmol/L on day 0 and < or = 10 follicles. INTERVENTIONS: Human GCs obtained during gonadotropin-releasing hormone agonist-pretreated IVF-GIFT cycles were cultured in the absence (control) or presence (hCG) of hCG, 1 IU/mL, and/or androstenedione (A) 10(-7) M. Granulosa cells obtained from follicles < or = 15 mm diameter were cultured separately from those obtained from follicles > 15 mm diameter. MAIN OUTCOME MEASURES: Estradiol (E2) and progesterone were measured in tissue-culture medium by a solid-phase direct radioimmunoassay. RESULTS: In vitro E2 production by cultured GCs was significantly increased in follicles < or = 15 mm diameter from women considered at risk of developing OHSS (group I). Estradiol response to hCG and/or A appeared enhanced in all follicles in group I. Progesterone production in the basal and hCG challenged state was greater in cells obtained from large follicles in group I than in group II. CONCLUSION: Ovarian hyperstimulation syndrome appears to be a function of an increased number of follicles that express an enhanced steroidogenic capacity.     

Leptin affects pregnancy outcome of in vitro fertilization and steroidogenesis of human granulosa cells

Purpose: This study was to examine the serum leptin levels in the prediction of pregnancy outcomes in women receiving ovarian hyperstimulation. Effect of leptin on the steroidogenesis was evaluated for granulosa cell (GC) culture in vitro. Method: Serum levels of leptin and estradiol were measured on Day 2, the time of hCG administration and oocyte retrieval in 50 women undergoing long-course GnRH agonist ovarian hyperstimulation. The production of estrogen and progesterone in granulosa cell culture were detected after administration of leptin at the absence or presence of FSH 1 mIU. Results: Leptin levels at the time of hCG injection were significantly lower in the pregnant women than in those without pregnancy. Estradiol concentrations were not correlated with leptin levels during the time of hCG injection and oocyte retrieval. High leptin concentration suppressed both basal estradiol and progesterone productions in GC. Leptin in high doses suppressed estradiol production, but did not alter progesterone production of GC in the presence of FSH. Conclusions: Serum leptin levels may be predictive of IVF pregnancy outcome with the effect on intraovarian progesterone/estradiol ratio during the follicular phase. Significantly low serum leptin levels were noted in the pregnant women than in the nonpregnant women.     

Effect of estradiol and progesterone on human chorionic gonadotropin secretion in vitro

Many of the substances known to control the secretion of pituitary gonadotropins also modulate the secretion of human chorionic gonadotropin (hCG) by the placenta. In order to study the effect of estrogens and progestins on hCG secretion, term placental explants were cultured in culture media for 144 hours. During the culture period, hCG secretion increased after 48 hours, and a fortyfold increase was observed after 144 hours (p less than 0.001). Compared to concentrations of hCG in control cultures, secretion of hCG was markedly suppressed in the presence of progesterone 2.25 X 10(-5)M (p less than 0.001), a concentration similar to that found in term placental tissue (1.7 +/- 0.2 micrograms/gm of tissue). Suppression of hCG by progesterone occurred in a dose-response manner (r = -0.9100, p less than 0.01). Estradiol, an important steroid modulator of pituitary gonadotropins, did not significantly suppress the secretion of hCG, except in pharmacologic concentrations (10(-4)M), and physiologic concentrations of estradiol had no effect on the suppression of hCG by progesterone. These results suggest that the mechanism by which progesterone suppresses the secretion of hCG differs from the manner in which steroids modulate the secretion of pituitary gonadotropins.