• The Journal of Korean Physical Therapy
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• v.21 no.2
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• pp.109-116
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• 2009

Purpose: $17\beta$-estradiol is the most active endogenous estrogen, which is related to favorable changes in the plasma lipid profile, to relaxation of the coronary vessels, and to a decrease in platelet aggregation and vascular smooth muscle cell migration. However, although the beneficial effect of estrogens on plasma lipoproteins (ie, lowering low-density lipoprotein and increasing high-density lipoprotein cholesterol) contributes to cardiovascular protection, it does not fully account for the protective effect, particularly in the application of physical therapy, including low frequency electrical stimulation. Methods: The aim of this study was to demonstrate the inhibition of stressors, such as endothelin-1 (ET-1), serotonin (5-hydroxytryptamine, 5-HT), prostaglandin $F2\alpha$ ($PGF2\alpha$), and a protein kinase C (PKC) activator 12-deoxyphorbol 13-isobutyrate (DPB), induced isometric tension by $17\beta$-estradiol in vascular smooth muscle strips, respectively. In addition, the effects of low frequency electrical stimulation at the meridian points (CV-3, -4, Ki-12, SP-6, LR-3, BL-25, -28, -32, -52) on the indirect antihypertensive effect were examined by monitoring the changes in the serum $17\beta$-estradiol concentration in healthy volunteers. Results: Isometric tension analysis showed that the responses of inhibited tension by $17\beta$-estradiol were similar to the same stressors in rat aortic smooth muscle strips. Furthermore, although the continued amplitude modulation (AM) type of electrical stimulation was not increased significantly by electrical stimulation, the current of the frequency modulation (FM) type of low frequency electrical stimulation increased the serum $17\beta$-estradiol concentration in normal volunteers. Conclusion: These results, in part, suggest that $17\beta$-estradiol has the capacity to supress stressor-induced muscle tension, and electrical stimulation, particularly current of the FM type, has a modulatory effect on the sex steroid hormones, particularly $17\beta$-estradiol, in healthy volunteers.

• Korean Journal of Veterinary Research
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• v.37 no.2
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• pp.311-319
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• 1997

The mechanisms of $estradiol-17{\beta}$ regulating growth of both normal and neoplastic cells are not clear until now. In studies using various estrogen-dependent breast cell lines, it is recently known that estrogen controls the cell growth by regulating the expression of growth factors and/or their receptors. In the present study, we investigated the effects of $estradiol-17{\beta}$on cell growth and IGF-I binding sites using primary cultured renal proximal tubule cells. We have obtained results as follows : $Estradiol-17{\beta}(10^{-9})$ has stimulatory effects in cell growth. Cotreatment of $estradiol-17{\beta}(10^{-9}M)$ and $IGF-I(5{\times}10^{-8}M)$ significantly increased the growth of primary rabbit renal proximal tubule cells compared to that of $estradiol-17{\beta}$ or IGF-I alone treated cells. In binding studies, we found that the binding of $^{125}IGF-I$ on cell membranes was incubation time- and temperature-dependent. Incubation at $37^{\circ}C$ results in higher binding of $^{125}IGF-I$ than that of $23^{\circ}C$ or $4^{\circ}C$. Maximum binding was observed at $37^{\circ}C$ between 30 and 60 minutes. The binding of $^{125}IGF-I$ to both control and $estradiol-17{\beta}-treated$ cells was inhibited by unlabelled $IGF-I(10^{-8}{\sim}10^{-12}M)$ in a concentration-dependent manner. However, EGF did not compete for $^{125}IGF-I$ binding at $10^{-8}{\sim}10^{-12}M$. IGF-I binding to the membranes from both control and $estradiol-17{\beta}-treated$ cells was also analyzed. We found that $estradiol-17{\beta}-treated$ cells exhibited higher binding activity for IGF-I. When $estradiol-17{\beta}$ or tamoxifen alone, or $estradiol-17{\beta}$ and tamoxifen cotreated cells were compared, the binding ratio of $^{125}I-IGF-I$ of $estradiol-17{\beta}-treated$ cell was significantly increased but was similar to control in both $estradiol-17{\beta}$ and tamoxifen cotreated cell. These results suggest that $estradiol-17{\beta}$ in part controls cell proliferation by regulating the expression of IGF-I receptors in primary rabbit renal proximal tubule cells.

• Biomedical Science Letters
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• v.14 no.3
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• pp.131-137
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• 2008

Adipogenesis is a complex sequence of events that culminates in the differentiation of fibroblast-like preadipocytes into specialized lipid-filled adipocytes and also involves a cascade of expression of many transcription factors such as peroxisome proliferator-activated receptor ${\gamma}(PPAR{\gamma})$ and CCAAT/enhancer-binding proteins (C/EBPs). $PPAR{\gamma}$ and C/EBPs transcriptionally transactivate adipocyte specific genes, including fatty acid transport protein (FAT/CD36) and leptin. To determine whether $17{\beta}$-estradiol modulates $C/EBP{\alpha}$ actions on adipogenesis in high fat diet-fed female ovariectomized (OVX) C57BL/6 mice, mice were treated with $17{\beta}$-estradiol for 7 days and the effects of $17{\beta}$-estradiol on adipose tissue mass and expression of adipocyte specific gene as well as $C/EBP{\alpha}$ were measured. Compared to vehicle-treated OVX control mice, OVX mice treated with $17{\beta}$-estradiol for 7 days had lower adipose tissue weights that were similar to weights in high fat diet-fed sham-operated (Sham) mice. OVX mice showed the increased expression of $C/EBP{\alpha}$ mRNA compared with Sham mice. However, $17{\beta}$-estradiol treatment in OVX mice inhibited OVX induced-$C/EBP{\alpha}$ activation, indicating that $17{\beta}$-estradiol may act as an inhibitor of $C/EBP{\alpha}$ action. Moreover, $17{\beta}$-estradiol decreased mRNA levels of adipocyte marker genes, such as lipoprotein lipase, FAT/CD36 and leptin, to levels in Sham mice. These results suggest that down-regulation of adipogenesis by $17{\beta}$-estradiol may be due to reduced adipose $C/EBP{\alpha}$ activities in female OVX C57BL/6 mice.

• Journal of Embryo Transfer
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• v.13 no.3
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• pp.291-300
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• 1998

This study was carried out to elucidate the effect of progesterone, estradiol 17 beta and cholesterol in follicular fluid on sperm chemotaxis for fertilization. By inducing swim-up migration through sucrose layer into bMSS containing progesterone, estradiol 17 beta and/or cholesterol, their effects on sperm migration and sperm movement were examined. And the results obtained were as follows; 1. Progesterone inhibited sperm migration and movement, but significantly attracted capacitated-sperm at the level of 50 $\mu$g/ml. 2. Estradiol 17 beta inhibited sperm migration and movement, but didn＇t significantly inhibit migration of capacitated-sperm at the level of 10$\mu$g/ml. 3. Cholesterol significantly stimulated sperm migration and movement at the level of 50$\mu$g/ml, but didn＇t attact capacitated-sperm. 4. Progesterone and estradiol 17 beta reduced the effect of cholesterol stimulating sperm migration and movement. But estradiol 17 beta and cholesterol didn＇t reduce the effect of progesterone attracting capacitated-sperm. In conclusion, progesterone of 50$\mu$g/ml in bMSS attracted the capacitated-sperm, cholesterol of 50$\mu$g/ml stimulated sperm migration and movement, but estradiol 17 beta of 10$\mu$g/ml didn＇t affect sperm swim-up separation.

• Journal of Aquaculture
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• v.4 no.2
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• pp.97-110
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• 1991

This study was undertaken to understand the seasonal changes of hormone levels such as luteinizing hormone (LH), follicle stimulating hormone (FSH) and estradiol-$17{\beta}$, serum components such as albumin, total protein and triglycerides, and GSI of rainbow trout (Onco-rhynchus mykiss) under the normal-light circumstances. LH levels were the highest in November whereas FSH levels were decreased progressively from October to February. Serum GTH, such as LH and FSH, levels were low immediately after egg-stripping and were significantly increased in the summer in association with the initiation of vitellogenesis. Serum albumin, total protein, and triglycerides were significantly increased in August in association with initiation of vitellogenesis and were peak in November prior to egg-stripping. Oocyte growth, measured by oocyte diameter and GSI, was significantly increased in August and showed the highest value in January. Correlation coefficients of serum LH with FSH and estradiol-$17{\beta}$ were +0.844 and +0.947, respectively. Correlation coefficients of estradiol-$17{\beta}$ with albumin and total protein were +0.634 and +0.859, respectively. Correlation coefficients of serum estradiol-$17{\beta}$ with triglycerides and GSI were +0.673 and +0.694, respectively. Probably by positive feedback mechanism, LH, FSH and estradiol-$17{\beta}$ appeared to stimulate to liver to secrete albumin, total protein and triglycerides for vitellosenesis.

• Ocean and Polar Research
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• v.32 no.4
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• pp.369-377
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• 2010

To characterize ecotoxicological responses to a natural estrogen, $17{\beta}$-estradiol, we evaluated the life-history of the parental ($F_0$) and first generation ($F_1$) of the harpacticoid copepod, Tigriopus japonicus sensu lato. We evaluated the survival of nauplii and copepodites, the number of days until the emergence of copepodites and adult males, the sex ratio, brooding success, and the first brooding day of adult females. No significant differences in the survival rate were noted in response to treatments with different concentrations of $17{\beta}$-estradiol. However, $17{\beta}$-estradiol induced developmental delay and skewed the sex ratio toward males. Copepod development was delayed significantly in the 0.1 and $1\;{\mu}g\;l^{-1}$ $17{\beta}$-estradiol treatment groups relative to the control group, with a more pronounced delay in the $F_1$ group. Body length and biomass were significantly smaller in the $17{\beta}$-estradiol treated groups than in the controls. The male emergence of T. japonicus s.l. was very high in the 10 and $30\;{\mu}g\;l^{-1}$ $17{\beta}$-estradiol treatment group. Furthermore, exposure to $17{\beta}$-estradiol resulted in morphological deformities such as shrinking and swelling of the urosome, twisted setae of the caudal rami, setal loss of swimming legs, abnormal segmentation of antennules, and dwarfism.

• Journal of Embryo Transfer
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• v.3 no.1
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• pp.13-23
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• 1988

These studies were undertaken to examine the interaction of tamoxifen with sex steroid hormones in rat uterine activity. The uterine wet weights of the immature Tat uterus were examined after the administration of estradiol-l7$\beta$(1$\mu$g), tamoxifen(50$\mu$g), progesterone(lmg). The uterotropic activity in immature ovariectomized rats was observed under various treatment conditions following pretreatment with above drugs. The results obtained were as follows:1) Tamoxifen produced significant increase (p <0.01) in uterine wet weight compared with control group, although the increase was not as great as that seen with estradiol-17$\beta$. Administration of estradiol-17$\beta$ together with tamoxifen inhibited significantly the increase of uterine wet weight by estradiol-17$\beta$ (p < 0.01). Coadministration of progresterone with tamoxifen partly blocked the increase of tamoxifen-induced uterine wet weights by progesterone. 2) Estradiol-17$\beta$after the estradiol-17$\beta$ pretreatment discontinued the declining uterine wet weights due to the absence of estrogen support, but uteri continued to increase in weight if daily estradiol-17 $\beta$ was maintained. Administration of tamoxifen on the fourth day of estradiol-17$\beta$ treatment reduced uterine wet weights within 24 hours, and the weights continued to decline with additional tamoxifen. 3) The modest growth of the uterus induced by three daily injections of 5Opg tamoxifen remained stable for five days, with or without additional tamoxifen treatment. Coadministration of tamoxifen with estradiol17$\beta$ increased slightly the increase of uterine wet weight by tamoxifen. Coadministration of tamoxifen with progesterone inhibited the increase of uterine wet weight by tamoxifen. 4) The modest growth of the uterus induced by three daily injections of lmg progesterone reduced uterine wet weight to the control level for five days. Commencement of tamoxifen or estadiol-17 $\beta$ injections on the fourth day of progesterone treatment rapidly elevated uterine wet weight.

• Biomedical Science Letters
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• v.19 no.2
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• pp.147-152
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• 2013

17-${\beta}$-hydroxysteroid dehydrogenase type 1 ($17{\beta}$-HSD type 1) mediates the reaction of $17{\beta}$-estradiol (E2) production from estrone (E1). Inhibitory effects of curcuminoids on $17{\beta}$-HSD type 1 activity were investigated to find a lead compound for treating estrogen-dependent diseases including breast cancer. Among curcuminoids, demethoxycurcumin showed potent inhibitory effect ($IC_{50}=2.7{\mu}M$) on mouse $17{\beta}$-HSD type 1. Curcuminoids also displayed their inhibitory effects on the production of $17{\alpha}$-estradiol which is a carcinogenic metabolite produced by the enzyme. Bisdemethoxycurcumin ($IC_{50}=1.3{\mu}M$) showed potent inhibitory effect on the $17{\alpha}$-estradiol production by chicken $17{\beta}$-HSD type 1. Curcuminoids did not inhibit ERE transcriptional activity with and without E2. Taken together, curcuminoids can be used for treating and preventing E2-dependent diseases via inhibition on $17{\beta}$-HSD type 1 activity.

• Korean Journal of Animal Reproduction
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• v.15 no.2
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• pp.117-124
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• 1991

This stduy was conducted to find out the changes of estradiol-17$\beta$ and progesterone levels in the plasma of Cheju mares during gestatation period and before and after parturition with 12 heads of Cheju ponies. The results are as follows : 1. The estradiol-17$\beta$ and progesterone levels on the 1~4 months showed 61.6~134.2pg/ml and 7.74~9.20ng/ml respectively, but the estradiol-17$\beta$ levels rapidly increased to 426.4~1772.9pg/ml, and the progesterone levels decreased to 1.42~5.43ng/ml on the 5~10 months of gestation period. 2. The progesterone levels of the pregnant and the non-pregnant mares showed 4.80ng/ml and 0.04ng/ml in winter, respectively, but both of the two appeared 1,211.5pg/ml and 99.4pg/ml of estradiol-17$\beta$, respectively. Therefore the diagnosis of pregnancy might be more accurate with the levels of estrdiol-17$\beta$ in autumn. 3. The progesterone levels showed 3.20ng/ml the day before parturition and less than 1ng/ml on 2 days after parturition. The estradiol-17$\beta$ levels, showing the rising trend, and 90.1~162.4pg/ml up to 10 days.

• Journal of Periodontal and Implant Science
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• v.29 no.3
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• pp.645-654
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• 1999

Interleukin-6(IL-6) stimulate osteoclast differentiation. $17{\beta}$-estradiol, 1,25-dihydroxyvitamin $D_3$(1,25-$(OH)_2D_3$) and interleukin-$1{\beta}$ inhibit or stimulate osteoclast differentiation by decreasing or increasing the synthesis of interleukin-6(IL-6) from stromal/osteoblastic cells, respectively. Periodontal ligament(PDL) cells reside between the alveolar bone and the cementum and have osteoblastic characteristics. To estimate the effect of $17{\beta}$-estradiol and 1,25$(OH)_2D_3$ on IL-6 production of PDL cells, PDL cells were treated with $17{\beta}$-estradiol or 1,25-$(OH)_2D_3$ in the absence or the presence of IL-$1{\beta}$. The concentration of IL-6 produced form PDL cells was determined by enzym linked immunosorbent assay(ELISA). In unstimulated PDL cells, we detected constitutive production of IL-6 at 1st and 2nd day. IL-$1{\beta}$ increased IL-6 synthesis at 1st day and 2nd day. $17{\beta}$-estradiol had no significant effect on the secretion of this cytokine, either constitutively or after stimulation with IL- $1{\beta}$(0.05 ng/ml). 1,25-$(OH)_2D_3$($10^{-8}M$) decreased not only constitutive IL-6 production but also IL-$1{\beta}$-induced IL-6 production at 2nd day. These results suggest that 1,25-$(OH)_2D_3$ may control IL-$1{\beta}$-induced osteoclast differentiation by decreasing IL-$1{\beta}$-induced IL-6 secretion of PDL cells.