• The Journal of Korean Physical Therapy
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• 제21권2호
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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.

• 대한수의학회지
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• 제37권2호
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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.

• 대한의생명과학회지
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• 제14권3호
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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.

• 한국수정란이식학회지
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• 제13권3호
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• pp.291-300
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• 1998

난포액에 함유되어 있는 steroids와 sterol이 수정에 참여하는 정자의 주화성에 미치는 영향을 밝히기 위하여, progesterone, estradiol 17 beta 및 cholesterol이 sucrose 층으로부터 정자의 swim-up 분리에 미치는 영향을 조사하였던 바 얻어진 결과는 다음과 같다. 1. Progesterone은 정자의 이동과 운동성을 억제하였으나 수정능획득한 정자를 유인하였으며, 특히 50$\mu$g/ml 수준의 progesterone은 수정능력을 획득한 정자의 이동을 유의하게 자극하였다. 2. Estradiol 17 beta의 첨가수준이 증가할수록 정자의 이동과 운동성이 억제되었으나, 10$\mu$g/ml 수준의 estradiol은 정자의 이동과 운동성 및 수정능획득정자의 이동에 영향을 미치지 않았다. 3. Cholesterol은 정자의 이동과 운동성을 자극하였으나, 수정능획득정자의 이동에 영향을 미치지 않았으며, 특히 50$\mu$g/ml 수준의 cholesterol은 정자의 이동과 운동성을 유의하게 자극하였다. 4. Progesterone, estradiol 및 cholesterol의 병용처리에서, cholesterol은 정자의 이동과 운동을 유의하게 자극하였으나, progesterone과 estradiol은 이러한 cholesterol의 효과를 감소시켰다. Progesterone은 수정획득 정자의 이동을 자극하였으나 estradiol이나 cholesterol은 progester-one의 이러한 효과를 억제하지 않았다. 결론적으로 progesterone은 50$\mu$g/ml 첨가수준에서 수정능력을 획득한 정자의 swim-up이동을 유의하게 자극하였으며, cholesterol은 50$\mu$g/m1 첨가수준에서 정자의 이동을 자극하였으나, estradiol은 10$\mu$g/m1 첨가수준에서 정자의 이동과 운동성에 영향을 미치지 않았다.

• 한국양식학회지
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• 제4권2호
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• pp.97-110
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• 1991

1989년 3월부터 1990년 2월까지 정상적인 광주기 상태에서 한달에 한번씩 채취된 무지개 송어 암컷의 혈청중 LH, FSH, estradiol-$17{\beta}$ 농도, albumin, globulin, triglycerides의 변화 그리고 GSI의 변화를 조사하였고, 각 호르몬과 혈청성분 그리고 GSI간의 상관관계를 알기 위하여 본 연구를 실시하였다. 본 연구에서 얻어진 결과는 다음과 같이 나타났다. 1. 혈청중 LH 수준은 11월에 가장 높게 나타났다. 2. 10월부터 그 이듬해 2월까지 혈청 LH 수준은 점차적으로 낮아지는 경향을 나타내었다. 3. LH 및 FSH와 같은 GTH의 수준은 인공산란직후 낮게 나타났고, 난황형성(vitellosenesis)이 개시되는 늦여름부터 유의하게 증가하였다. 4. 혈청중 FSH 수준은 LH와 estradiol-$17{\beta}$에 대해서 고도의 유의성(P<0.001)을 나타내었다. 5. 혈청중 LH는 estradiol-$17{\beta}$에 대해서 고도의 유의성(P<0.001)을 나타내었다. 6. negative feedback mechanism에 의해서 2월에 estradiol-$17{\beta}$의 수준이 감소하였다. 7. 혈청중 albumin과 total protein의 함량은 난황형성이 개시되는 8월에 유의성있게 증가하다가 산란직전인 11월에 가장 높은 수준을 나타내었다. 8. 혈청중 triglycerides 함량은 8월에 유의하게 증가하였고, 1월에 최고 수준을 나타내었다. 9. 난직경 및 GSI의 크기로 나타나는 난모세포의 성장은 8월에 유의성있게 증가하다가 산란시기인 1월에 최고 수준을 나타내었다. 10. 혈청중 LH와 FSH와의 상관계수는 +0.844이다. 11. 혈청중 LH와 estradiol-$17{\beta}$와의 상관계수는 +0.947이다. 12. 혈청중 FSH와 estradiol-$17{\beta}$와의 상관계수는 +0.894이다. 13. 혈청중 estradiol-$17{\beta}$와 albumin과의 상관계수는 +0.634이다. 14. 혈청중 estradiol-$17{\beta}$와 total protein의 상관계수는 +0.947이다. 15. 혈청중 LH와 GSI와의 상관계수는 +0.506이다. 16. 혈청중 FSH와 estradiol-$17{\beta}$와의 상관계수는 +0.586이다. 17. 혈청중 estradiol-$17{\beta}$와 GSI와의 상관계수는 +0.694이다. 18. 혈청중 LH와 total protein과의 상관계수는 +0.947이다. 19. 혈청중 FSH와 total protein과의 상관계수는 +0.709이다. 20. 혈청중 FSH와 triglycerides와의 상관계수는 +0.549이다. 21. 혈청중 estradiol-$17{\beta}$와 triglycerides와의 상관계수는 +0.673이다. 22. positive feedback mechanism에 의해서 LH, FSH와 estradiol-$17{\beta}$는 간을 자극시켜 albumin, total protein 및 triglycerides를 분필시킴으로서 난황형성(vitellosenesis)에 관여하는 것으로 나타났다.

• Ocean and Polar Research
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• 제32권4호
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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.

• 한국수정란이식학회지
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• 제3권1호
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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.

• 대한의생명과학회지
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• 제19권2호
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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.

• 한국가축번식학회지
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• 제15권2호
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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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• 제29권3호
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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.