Association between serum estradiol level and appendicular lean mass index in middle-aged postmenopausal women

BACKGROUND Previous studies investigating the association between loss of estrogen at menopause and skeletal muscle mass came to contradictory conclusions.AIM To evaluate the association between serum estradiol level and appendicular lean mass index in middle-aged postmenopausal women using population-based data.METHODS This study included 673 postmenopausal women,aged 40-59 years,from the National Health and Nutrition Examination Survey between 2013 and 2016.Weighted multivariable linear regression models were used to evaluate the association between serum E2 Level and appendicular lean mass index(ALMI).When non-linear associations were found by using weighted generalized additive model and smooth curve fitting,two-piecewise linear regression models were further applied to examine the threshold effects.RESULTS There was a positive association between serum E2 level and ALMI.Compared to individuals in quartile 1 group,those in other quartiles had higher ALMI levels.An inverted U-shaped curve relationship between serum E2 Level and ALMI was found on performing weighted generalized additive model and smooth curve fitting,and the inflection point was identified as a serum E2 level of 85 pg/mL.CONCLUSION Our results demonstrated an inverted U-shaped curve relationship between serum E2 levels and ALMI in middle-aged postmenopausal women,suggesting that low serum E2 levels play an important in the loss of muscle mass in middleaged postmenopausal women.

Effects of Ovariectomy and 17β-Estradiol Replacement on the Activity of Dopamine D2 Receptors in the Selection of Macronutrients Carbohydrates, Lipids and Proteins in Females Rats

17β-estradiol modulates the activity of D2 receptors in the regulation of food intake and body weight. The functional lack of 17β-estradiol in postmenopausal women could create a dietary imbalance and cause body weight gain. This study aimed to better understand the interferences that could exist between 17β-estradiol, D2 receptors and the selection of carbohydrate, fat and protein consumption, as well as their consequences on body weight gain by using an animal model of the menopause. Ovariectomy exacerbates the consumption of foods rich in lipids. Thus confirming an inhibitory action of 17β-estradiol (E2) on the consumption of these types of foods. This consumption stimulates body weight gain, which is promoted by the high caloric content of these foods and not by the amount consumed. Our results showed a direct involvement of D2 receptors in food choice. This choice would be made according to the two (2) isoforms of the D2 receptors. The D2/BR isoform directs towards a high carbohydrate consumption, without causing a gain in body weight. While D2/SUL, promotes high fat food consumption, causing an increase in body weight. In women, 17β-estradiol modulates the activity ratio between these two D2 receptor isoforms to ensure energy and homeostatic balance, stabilizing food intake and body weight.

Formestane和17-βestradiol诱导鸡、鹌鹑胚胎性反转的研究

为了研究芳香化酶抑制剂(Formestane)和17β-雌二醇(17-βestradiol)对鸡和鹌鹑胚胎性分化的影响,试验根据家禽性别分化的机理,利用100μg/mL的Formestane和50μg/mL的17-βestradiol,通过胚蛋注射的方法对3日龄的鸡胚和2日龄的鹌鹑胚进行处理,观察Formestane和17-βestradiol对鹌鹑性别分化的影响。结果表明,注射Formestane和17-βestradiol的鸡胚和鹌鹑胚都发生了性反转。

17β-estradiol配伍DRSP对绝经综合征患者血清FSH及E2调控作用

目的 研究17β-estradiol配伍DRSP治疗绝经综合征患者血清FSH及E2调控作用。方法 选取2013年11月~2016年11月在丽水市人民医院接受治疗的绝经综合征的女性患者共90例。随机将患者分为3组,17β组（30例,单独使用17β-estradiol治疗）、DRSP组（30例,单独使用DRSP治疗）、联合组（30例,17β-estradiol结合DRSP治疗）。使用Kupperman的绝经综合征的评测法,对患者的身体症状量化,治疗后对患者进行比较分析,观察3组患者的治疗有效率情况,患者在治疗前进行的检查项目包含肝肾功能、血尿常规、空腹时血糖含量、卵泡刺激素（follicle-stimulating hormone,FSH）、E2、低密度脂蛋白（low-density lipoprotein,LDL）、总胆固醇（total cholesterol,TC）、心电图、腔内的多普勒超声、乳腺的彩超、高密度脂蛋白（high-density lipoprotein,HDL）等,治疗前按照Kupperman评测表评价一次,在每个疗程结束后再测量一次,并在此进行上述的各项检查。结果 联合组患者在治疗后,除了皮肤上的蚁走感和治疗前没有差异以外,其他的症状的积分差异均都统计学的意义,其中性交痛、头痛、身体感觉异常、容易激动、心悸、关节痛、疲乏、失眠和潮热的症状评分差异显著（P〈0.01）,DRSP组患者在治疗后,性交痛、抑郁和失眠有所改善,差异有统计学意义（P〈0.05）,其他症状均无明显改善;17β组患者在治疗后,头痛、关节疼痛和失眠有所改善,差异有统计学意义（P〈0.05）,其他症状均无明显改善;联合组的总有效率为90.0%,DRSP组的总有效率为73.33%,17β组的总有效率为70.0%,联合组与另外量组对比差异显著（P〈0.05）,治疗前后联合组患者在血TC、E2和FSH对比中差异显著（P〈0.05）,DRSP组患者FSH在治疗前后有差异,其他均无差异,17β组患者E2在治疗前后有差异,其他均无差异。结论 17β-estradiol配伍DRSP治疗绝经综合征患者取得了良好的临床疗效,其体内血清FSH及E2调控作用显著。

Association of 2-methoxyestradiol levels with the occurrence and development of endometrial cancer in humans

Objective The aim of the study was to determine the association of urinary levels of estradiol(E_(2))and 2-methoxyestradiol(2-MeOE_(2))with the occurrence and development of endometrial cancer.Methods In this case-control study,24-h urine specimens were collected from 28 postmenopausal patients with endometrial cancer and 28 postmenopausal healthy female controls.The concentration of 2-MeOE_(2) was determined using liquid chromatography-mass spectrometry with hollow fiber liquid-phase microextraction.The concentration of E_(2) was determined using an enzyme-linked immunosorbent assay.Results Estrogen levels were different between the patients with endometrial cancer and controls.The relative quantity of E_(2) in the case group was higher than that in the control group(P<0.05),whereas that of 2-MeOE_(2) was lower in the case group than that in the control group(P<0.05).The ratio of E_(2)-to-2-MeOE_(2) in the case group was significantly higher than that in the control group(P<0.05).Conclusion The results of this study indicate an imbalance of estrogen metabolites in endometrial carcinogenesis.Reduced 2-MeOE_(2) levels and elevated E_(2)-to-2-MeOE_(2) ratio may be used as potential biomarkers for the risk assessment of estrogen-induced endometrial cancer.

17β-estradiol通过促进PSD95/nNOS耦联抑制皮层海马神经元的存活

目的:检测17β-estradiol对皮层海马神经元存活的影响,并判断其与nNOS/PSD95耦联的关系。方法:采用原代培养的ICR小鼠皮层海马神经元,培养7天后分溶剂对照组和给药组分别给予溶剂DMSO和浓度为10μmol/L的17β-estradiol,LDH法判断细胞损伤,测定给药30 min后细胞死亡情况,并拍摄光镜照片观察细胞形态。同时利用免疫共沉淀法检测DMSO组,10nmol/L17β-estradiol组,10μmol/L 17β-estradiol组的nNOS和PSD95的耦联情况,观察药物对其影响。结果:给药30 min后,与对照组相比,10μmol/L17β-estradiol组LDH漏出率增加,同时nNOS/PSD95耦联增加,而10 nmol/L 17β-estradiol对nNOS/PSD95耦联并没有影响。结论:浓度为10μmol/L的17β-estradiol会损伤皮层海马神经元,而且这一结果可能是通过促进nNOS/PSD95耦联实现的。

The protective effect of 17 beta-estradiol on oxygen-induced retinopathy and its relation with the changes of malondialdehyde

Objective： Retinopathy of prematurity is becoming obvious with the improvement of neonatal ambulance. However there is still not a good treatment. The present study is to observe the effect of 17 beta-estradiol （E2） on oxygen-induced retinopathy （OIR）, and explore the relationship between the changes of avascular area and malondialdehyde （MDA） in retina. Methods： Newborn oxygen-exposed mice underwent subcutaneous injections of different dose of E2 （0.1 μg, 1.0 μg, 10.0 μg ）, tamoxifen or phosphate buffered saline （PBS; controls）everyday from post-natal day （p）7 to p17. At p17, retinal flat mounts were scored for the percentage of avascular/total retinal area, and pathological changes during revascularization. The MDA concentration in the retina was determined also. In the most efficacious E2 group （10.0 μg）, 100.0 μg tamoxifen was also administered, and the percentage of capillary-free/total retinal area determined, and the retinal malondialdehyde concentration assayed. Results： The mean percentage of capillary-free area over total retinal area was 0（PBS, in room air）, 34.197±1.301（PBS, in hyperoxia）, 23.685±0.407 （0.1 μg E2）, 14.648±0.355 （1.0 μg E2）, 4.693±0.450 （10.0 μg E2） and 32.240±0.654 （10.0 μg E2 ＋100.0 μg tamoxifen）. The difference was significant （F = 2778.759, P 〈 0.01）, and the difference between any two groups were also significant （all P value were less than 0.01）. The predilection of tufts and clusters during revascularization was mainly aggregated in zones 2 and 3, but the difference of retinal neovascular clusters and tufts in fourth zone among different groups were significant [clusters （F = 44.719, P 〈 0.01） vs tufts （F = 39.997,P 〈 0.01）]. The mean MDA concentration were 0.711 ±0.037（PBS, in room air）, 2.084±0.066 （PBS, in hyperoxia）, 1.829±0.091（0.1 μg E2）, 1.152± 0.067（1.0 μg E2）, 0.796 ±0.027（10.0 μg E2）, 1.988 ± 0.049（10.0μg E2 ＋100.0 μg tamoxifen） （F = 628.103, P 〈 0.01）. The difference between any two groups were also significant （all P value were less than 0.05）. The close relation between the percentage of avascular/total retinal area and MDA concentration was also verified （r = 0.981, P 〈 0.01）. Conclusion： Oxidative stress responses play a pivotal role in OIR, by means of receptor pathway. E2 can alleviate oxidative stress reaction, and thus ameliorate the severity of oxygen induced retinopathy.

Maturation, proliferation and apoptosis of seminal tubule cells at puberty after administration of estradiol, follicle stimulating hormone or both

Aim： To assess proliferative and apoptotic potential of the seminiferous epithelium cells in relation to Sertoli cell maturation in newborn rats under the influence of estradiol, follicle stimulating hormone （FSH） or both agents given together. Methods： From postnatal day （PND） 5 to 15 male rats were daily injected with 12.5 μg of 1713-estradiol benzoate （EB） or 7.5 IU of human purified FSH （hFSH） or EB ＋ hFSH or solvents （control）. On postnatal day 16, autopsy was performed. Sertoli cell maturation/function was assessed by morphometry. Proliferation of the seminiferous epithelium cells was quantitatively evaluated using immunohistochemical labeling against proliferating cell nuclear antigen and apoptosis using the TUN-EL method. Results： Although EB inhibited Sertoli cell maturation and hFSH was not effective, a pronounced acceleration of Sertoli cell maturation occurred after EB ＋ hFSH. Whereas hFSH stimulated Sertoli cell proliferation, EB or EB ＋ hFSH inhibited Sertoli cell proliferation. All treatments significantly stimulated germ cell proliferation. Apoptosis of Sertoli cells increased 9-fold and germ cells 2-fold after EB, and was not affected by hFSH but was inhibited after EB ＋ hFSH. Conclusion： At puberty, estradiol inhibits Sertoli cell maturation, increases Sertoli and germ cell apoptosis but stimulates germ cell proliferation. Estradiol in synergism with FSH, but neither of the hormones alone, accelerates Sertoli cell maturation associated with an increase in germ cell survival. Estradiol and FSH cooperate to induce seminal tubule maturation and trigger first spermatogenesis.

MiR-214-3p promotes proliferation and inhibits estradiol synthesis in porcine granulosa cells

Background: Granulosa cells(GCs) proliferation and estradiol synthesis significantly affect follicular development.The miR-214-3p expression in the ovarian tissues of high-yielding sows is higher than that in low-yielding sows,indicating that miR-214-3p may be involved in sow fertility. However, the functions and mechanisms of miR-214-3p on GCs are unclear. This study focuses on miR-214-3p in terms of the effects on GCs proliferation and estradiol synthesis.Results: Our findings revealed that miR-214-3p promotes proliferation and inhibits estradiol synthesis in porcine GCs. MiR-214-3p can increase the percentage of S-phase cells, the number of EdU labeled positive cells, and cell viability. However, E2 concentration was reduced after miR-214-3p agomir treatment. We also found that miR-214-3p up-regulates the expression of cell cycle genes including cell cycle protein B(Cyclin B), cell cycle protein D(Cyclin D), cell cycle protein E(Cyclin E), and cyclin-dependent kinase 4(CDK4) at the transcription and translation levels, but down-regulates the mRNA and protein levels of cytochrome P450 family 11 subfamily A member 1(CYP11A1), cytochrome P450 family 19 subfamily A member 1(CYP19A1), and steroidogenic acute regulatory protein(StAR)(i.e., the key enzymes in estradiol synthesis). On-line prediction, bioinformatics analysis, a luciferase reporter assay, RT-qPCR, and Western blot results showed that the target genes of miR-214-3p in proliferation and estradiol synthesis are Mfn2 and NR5A1, respectively.Conclusions: Our findings suggest that miR-214-3 p plays an important role in the functional regulation of porcine GCs and therefore may be a target gene for regulating follicular development.

Calcium potentiates the effect of estradiol on PGF2α production in the bovine endometrium

Background： Estradiol （E2） is required for luteolysis in cows and its injection stimulates prostaglandin F2α （PGF2α） release. The main goal of our study was to investigate the ability of endometrial explants and cells treated with E2 and the calcium ionophore （CI） A23187 to synthesize PGF2α. Results： Treatment with E2 in vivo resulted in a 48.4% increase of PGF2α production by endometrial explants treated in vitro with A23187. Production of PGF20 was better stimulated with A23187 at concentrations of 10^-6 and 10^-5 mol/L compared with other concentrations used. The concentration of PGF2α for untreated bovine endometrial cell cultures was 33.1 pg/mL, while for cultures treated with E2, A23187, or a combination of E2 and A23187, the PGF2α concentration was 32.5, 92.4 and 145.6 pg/mL, respectively. Conclusions： Treatment with A23187 tended to stimulate PGF20 production. In the presence of E2, A23187 significantly stimulated PGF20 synthesis. It appears that A23187 potentiates the effects of E2 with respect to synthesis of endometrial PGF2α in cattle.

17β-Estradiol Regulates Cultured Immature Boar Sertoli Cell Proliferation via the cAMP-ERK1/2 Pathway and the Estrogen Receptor β

Estrogen plays an important role in regulating Sertoli cell number in the testis. The objective of the study was to identify whether 17β-estradiol affected the proliferation of cultured, immature boar Sertoli cells via the estrogen receptor β （ERβ） and the cAMP-extracellular signal-regulated kinase （ERK1/2） pathway. Low levels （10-10-10-8 mol L-1） of 17β-estradiol increased cell number, but high levels （10-7-10-6 mol L-1） decreased it （P〈0.05）. Sertoli cell number began to recover for an additional 24 h in the medium without 17β-estradiol （10-6 mol L-l） （P〉0.05）. The effects of 17β-estradiol （10-9 mol L-1） peaked at the first 24 h （P〈0.05）. 17β-estradiol activated ERK1/2 from 5 min to 24 h, but the activiy of ERK1/2 began to decrease after 4 h. Both PD98059 and U0126, two ERK inhibitors, blocked cell division （P〈0.05）. 17β-estradiol （10-10-10-6 mol L-1） dose-dependently increased cAMP production （P 〈 0.05）, and both 17β-estradiol （10-9 mol L-1） and forskolin, which increases cAMP levels, induced cell proliferation and activated ERK1/2 （P〈 0.05）. Rp-cAMP, an antagonist of cAMP, blocked this 17β-estradiol activity （P〈 0.05）. Two estrogen receptor antagonists, ICI 182780 and ERβ antagonist （ERβAnt）, reduced Sertoli cell number, cAMP production and ERK1/2 activation （P〈 0.05）, but ERaAnt did not （P〉 0.05）. Therefore, 17β- estradiol mainly promotes pig Sertoli cell proliferation via ERβ to induce cAMP production and ERK activation to promote cell proliferation.

Effects of estradiol-17β and bisphenol A administered chronically to mice throughout pregnancy and lactation on the male pups＇ reproductive system

Aim： To assess the effect of estradiol-17β （E2） and bisphenol A （BPA） administered chronically by implanting a silicone tube throughout pregnancy and lactation on male pups＇ reproductive system in ICR mice. Methods： Female mice were implanted with a tube filled with 10 ng, 500 ng, 1 μg, or 10 μg of E2, or 100 μg or 5 mg of BPA, before mating. The tube was kept in the mice throughout pregnancy and lactation, until the pups had weaned at 4 weeks of age. During the period, E2 was released from the tube at 120 pg or 6, 12 or 120 ng/day, and BPA at 1.2 or 60 μg/day. Results： Most of the mice given 1 μg and 10 lag of E2 did not maintain their pregnancy. However, the other groups showed high rates of birth, more than 70%. At age of 4 weeks, the male pups were killed. Body weight and reproductive organ weights （testes, epididymides and accessory reproductive glands） in the treated groups did not differ from the control values, whereas the percentage of seminiferous tubules in the testis with mature spermatids was significantly lower in the groups given 10 ng and 500 ng of E2 and 5 mg of BPA than that in the control. Conclusion： Chronic exposure to E2 and BPA might disrupt spermatogenesis in male pups. （Asian JAndrol 2008 Mar; 10： 271-276）

Differentially expressed genes and signalling pathways are involved in mouse osteoblast-like MC3T3-E1 cells exposed to 17-β estradiol

Oestrogen is essential for maintaining bone mass, and it has been demonstrated to induce osteoblast proliferation and bone formation.In this study, complementary DNA（cDNA） microarrays were used to identify and study the expression of novel genes that may be involved in MC3T3-E1 cells’ response to 17-b estradiol. MC3T3-E1 cells were inoculated in minimum essential media alpha（a-MEM）cell culture supplemented with 17-b estradiol at different concentrations and for different time periods. MC3T3-E1 cells treated with1028mol？L2117-b estradiol for 5 days exhibited the highest proliferation and alkaline phosphatase（ALP） activity; thus, this group was chosen for microarray analysis. The harvested RNA was used for microarray hybridisation and subsequent real-time reverse transcription polymerase chain reaction（RT-PCR） to validate the expression levels for selected genes. The microarray results were analysed using both functional and pathway analysis. In this study, microarray analysis detected 5 403 differentially expressed genes,of which 1 996 genes were upregulated and 3 407 genes were downregulated, 1 553 different functional classifications were identified by gene ontology（GO） analysis and 53 different pathways were involved based on pathway analysis. Among the differentially expressed genes, a portion not previously reported to be associated with the osteoblast response to oestrogen was identified. These findings clearly demonstrate that the expression of genes related to osteoblast proliferation, cell differentiation, collagens and transforming growth factor beta（TGF-b）-related cytokines increases, while the expression of genes related to apoptosis and osteoclast differentiation decreases, following the exposure of MC3T3-E1 cells to a-MEM supplemented with 17-b estradiol. Microarray analysis with functional gene classification is critical for a complete understanding of complementary intracellular processes. This microarray analysis provides large-scale gene expression data that require further confirmatory studies.

Crystal Structures and Physicochemical Properties of Solvated Estradiol

Polymorph screening is currently one of the most important tasks for innovators and for generic companies from both pharmaceutical and intellectual property rights aspects. The hemihydrate form（Form Ⅰ） and formamide solvate（Form Ⅱ） of estradiol are isolated and prepared via systemic crystallization screening in this paper, and the formamide solvate form is reported for the first time. Both polymorphic forms were characterized by single-crystal X-ray structure analysis（SXRD）, powder X-ray diffraction（PXRD）, and thermal analysis（TGA and DSC）. The PXRD experiments indicate that the samples in this study are the pure polymorphic forms via comparing the patterns with the simulated ones. The stability and equilibrium solubility data of the solid-state phase were also examined in order to check the impact of the differences observed in their crystalline structures. It has been found that Forms I and II are of conformational polymorph and Form II is the more thermodynamically stable solid form, while Form I possesses higher solubility, indicating its possibility as an alternate solid form for its further solid formulation development if necessary.

17beta-estradiol stimulates proliferation of spermatogonia in experimental cryptorchid mice

Aim： To investigate whether estrogen stimulates the proliferation of spermatogonia or induces spermatogenesis in cryptorchid mice. Methods： Mice were surgically rendered cryptorchid, then treated with different doses of 17β- estradiol （E2） s.c. once a day. Mice were killed at sexual maturity （45 days of age）, and histological analysis and inununofluorescence were performed. Serum follicle stimulating hormone （FSH）, estradiol, testosterone and luteinizing hormone （LH） were measured. Results： Low doses of E2 had no notable effect on spermatogonia, but at higher doses, E2 stimulated the proliferation of spermatogonia. Conclusion： E2 has a dose-related mitogenic effect on spermatogonia.

Simultaneous Determination of Hexoestrol, Diethylstilbestrol, Estrone and 17-Beta-estradiol in Feed by Gas Chromatography-mass Spectrometry

A method was developed for the simultaneous determination of four kinds of estrogens （hexoestrol, diethylstilbestrol, estrone, and 17-beta-estradiol） in feed by gas chromatography-mass spectrometry （GC-MS）. After the sample was extracted by ethyl ether and cleaned-up on HLB phase extraction column, four kinds of estrogens were derived and quantified in gas chromatographymass spectrometry. The results showed that the linear detectable ranged from 2.5 ng· mL-1 to 250 ng· mL-1for hexoestrol and from 5 ng· mL-1 to 500 ng· mL-1 for three other estrogens with the correlation coefficients （R2） were no less than 0.990. The recoveries were in the range of 76.34%-96.33% and the relative standard deviation was no more than 22.7%. The limits of quantitation （LOQ） for all analytics were between 10 ug· kg^-1 and 20 ug· kg^-1. The method was accurate and sensitive and could meet the actual requirements for the analyses of feed samples.

Novel estradiol sensors based on carbon nanotube multilayer modified gold hair microelectrodes

Multi-walled carbon nanotube multilayers were modified onto a newly proposed gold hair microelectrode via a simple layer-bylayer assembling method. The resulting electrode showed a sensitive oxidation response to estradiol with detection limit as low as 1.0 × 10^-8 mol/L, foreseeing a promising approach to the fabrication of high-sensitive microsensors.

Xenoestrogens challenge 17β-estradiol protective effects in colon cancer

Several epidemiological,cellular,and molecular studies demonstrate the role of environmental chemicals with endocrine disrupting activities,typical of Westernized societies,in the pathogenesis of numerous diseases including cancer.Nonetheless this information,the design and execution of studies on endocrine disruptors are not yet cognizant that the specific actions of individual hormones often change with development and ageing,they may be different in males and females and may be mediated by different receptors isoforms expressed in different tissues or at different life stages.These statements are particularly true when assessing the hazard of endocrine disruptors against 17β-estradiol(E2)actions in that this hormone is crucial determinant of sexrelated differences in anatomical,physiological,and behavioral traits which characterize male and female physiology.Moreover,E2 is also involved in carcinogenesis.The oncogenic effects of E2 have been investigated extensively in breast and ovarian cancers where hormone-receptor modulators are now an integral part of targeted treatment.Little is known about the E2preventive signalling in colorectal cancer,although this disease is more common in men than women,the difference being more striking amongst pre-menopausal women and age-matched men.This review aims to dissect the role and action mechanisms of E2 in colorectal cancer evaluating the ability of estrogen disruptors(i.e.,xenoestrogens)in impair these E2 actions.Data discussed here lead to define the possible role of xenoestrogens in the impairment and/or activation of E2signals important for colorectal cancer prevention.

Effects of Estradiol and Tamoxifen on Proliferation of Human Breast Cancer Cells and Human Endometrial Cells

The effects of estradiol and tamoxifen on the proliferation of estrogen receptor positive cells and the relationship between the tamoxifen tolerance and cell origin were investigated The tissues of human endometrium and breast cancer were randomly selected following dissection for primary cell culture After the breast cancer cells and endometrial cells were treated with 1×10 -8 mol/L estradiol and/or 1 ×10 -6 tamoxifen, 3H-labelled thymine nucleotide was used to trace the kinetics of cell proliferation There was no significant difference in the inhibition on the human endometrial cells between tamoxifen-treated group (6 3%) and control group (6 4%), but tamoxifen could significantly inhibit the proliferation of the human breast cancer cells (45 84%) as compared with control group (52 72%) Moreover, tamoxifen could significantly stimulate the proliferation of tamoxifen resistant breast cancer cells (9 64%) as compared with control group (6 32%) Estradiol could significantly stimulate the proliferation of all the three kinds of cells as compared with control group The combined use of estradiol and tamoxifen could inhibit the proliferation of the endometrial cells and breast cancer cells as compared with estradiol used alone, but on the tamoxifen resistant breast cancer cells, they could more significantly stimulate the proliferation than E2 It was concluded that E2 could stimulate the proliferation of these three kinds of cells However, the inhibitive effects of tamoxifen on the proliferation of these cells were dependent on the estradiol

Screening,Preparation,Characterization and Solubility of Polymorphic Forms of Ethinyl Estradiol

Ethinyl estradiol（EE） as a contraceptive,（17α）-19-nopregna-1,3,5-（10）-trien-20-yne-3,17-diol（formula： C（20）H（24）O2, molecular weight： 296.4, CAS number： 57-63-6）, is known to have different pseudo-polymorphic forms. Some EE polymorphs have been synthesized by means of physical or chemical methods, characterized by X-ray powder diffraction（XRPD）, thermogravimetric（TG）, differential scanning calorimetry（DSC） and IR spectra. Dissolution profile was tested by high performance liquid chromatography（HPLC）. Meanwhile, the crystal structure of the new EE solvate（formamide） was characterized by single-crystal X-ray structure analysis（SXRD）. The results confirmed that EE existed polymorphism. Five crystal forms of EE were presented and two of them were reported firstly. Furthermore, five polymorphs＇ dissolution curves were drawn and they could be identified by several analysis methods. Our study on polymorphs of EE could provide a variety of crystal material composition, preparation methods and solubility.