• 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.

• 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.

• 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.

• Reproductive and Developmental Biology
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• v.35 no.3
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• pp.215-219
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• 2011

Acyl-CoA synthetase 4(ACSL4) is an arachidonate-preferring enzyme abundant in steroidogenic tissues and postulated to modulate eicosanoid production. The human and mouse ACSL4 gene are mapped on chromosome X. The female mice heterozygous for ACSL4 deficiency became pregnant less frequent1y and produced small litters, with 40% of embryos surviving gestation. In this study, we examined the regulation of ACS4 by estradiol-$17{\beta}$ and progesterone (P4) in the human endometrial cancer cell line HTB-1B. ACSL4 mRNA was increased in a dose-dependent manner. Also, expression of ACSL4 gene was up-regulated in a time-dependent manner in HTB-1B cells. However, combined treatment with progesterone and estradiol-$17{\beta}$ modestly decreased the levels of ACS4L mRNA as compared with the estradiol-$17{\beta}$ and progesterone respectively. Overall, these results suggest that the ACSL4 gene is regulated by progesterone and estradiol-$17{\beta}$ in the HTB-1B cells.

• Journal of fish pathology
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• v.19 no.3
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• pp.189-195
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• 2006

A subtracted cDNA library of a marine scuticociliate, Philasterides dicentrarchii, in response to 17β-estradiol exposure was constructed using suppression subtractive hybridization (SSH). As a result of SSH, 275 clones were isolated, and among them, only glutathione peroxidase (GPX) gene was isolated as an antioxidative enzyme responding to 17β-estradiol. The semi-quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) analysis revealed that the transcription of GPX gene of P. dicentrarchii was clearly increased by exposure to 17β-estradiol. The GPX transcription was also clearly increased by exposure to xenoestrogens such as bisphenol A (BPA) and genistein.

• Biomedical Science Letters
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• v.13 no.2
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• pp.99-104
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• 2007

To determine whether 17$\beta$-estradiol induces the morphological changes in adipose and liver tissues, we measured the effects of 17$\beta$-estradiol on adipose tissue mass, adipocyte histology and hepatic lipid accumulation in female ovariectomized (OVX) C57BL/6J mice. Compared to vehicle-treated control mice, 17$\beta$-estradiol-treated mice decreased adipose tissue mass and the size of adipocytes, and concomitantly increased the number of adipocytes in a dose-dependent manner. In addition, the administration of 17$\beta$-estradiol resulted in reduced hepatic lipid accumulation in a dose-dependent manner. These results suggest that estrogen may regulate adipocyte development and lipid metabolism in female OVX C57BL/6J mice.

• 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.

• Korean Journal of Veterinary Research
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• v.27 no.1
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• pp.9-17
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• 1987

The present study has been carried out to elucidate the antiestrogenic effects of tamoxifen in immature rat uterus. The content of DNA and protein and uterine wet weight were measured after the injections of $5{\mu}g$ of estradiol-$17{\beta}$, $50{\mu}g$ of tamoxifen, a combination of both, or vehicle only subcutaneously. The results obtained were summarized as follows: 1. DNA content in uterus was increased at 48 hours after estradiol-$17{\beta}$ or tamoxifen injection (p<0.01). 2. The increament rate of uterine DNA content was significantly (p<0.01) lower in tamoxifen treated group than that in estradiol-$17{\beta}$ treated group. 3. Antiestrogenic effect of tamoxifen on protein content in uterus was apparent at 72 hours after simultaneous administration of both drugs. 4. The uterine wet weight was started to increase at three hours after the injection of estradiol-$17{\beta}$ or tamoxifen. 5. While estradiol-$17{\beta}$ increased steadily uterine wet weight up to 138.5mg at 72 hours after the injection, but tamoxifen failed to increase it after 48 hours. Tamoxifen inhibited significantly (p<0.01) the effect of estradiol-$17{\beta}$ on it thereafter.