• 대한의생명과학회지
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• 제15권3호
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• pp.179-185
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• 2009

In our previous report, we showed that $PPAR{\gamma}$ does not influence adipogenesis in females with functioning ovaries, indicating that $PPAR{\gamma}$ activity on adipogenesis is associated with sex-related factors. Among the sex-related factors, estrogen has been recognized as a major factor in inhibiting adiposgenesis in females. Thus, we hypothensized that $17{\beta}$-estradiol (E) inhibits 3T3-L1 cell adipogenesis by preventing $PPAR{\gamma}$ activity. E decreased triglyceirde accumulation in differentiated 3T3-L1 cells compared with control group. E also decreased the expression of $PPAR{\gamma}$ mRNA as well as $PPAR{\gamma}$ dependent adipocyte-specific genes, such as adipocyte fatty acid binding protein and tumor necrosis factor $\alpha$. In addition, E not only decreased luciferase reporter activity by $PPAR{\gamma}$, but also transfection of estrogen receptor $\alpha$ ($ER{\alpha}$) or $ER{\beta}$ led to decreases in $PPAR{\gamma}$ reporter gene activation. Moreover, E-activated ERs significantly decreased the luciferase reporter gene activation induced by $PPAR{\gamma}$ transfection, suggesting that estrogen-activated ERs inhibit $PPAR{\gamma}$-dependent transactivation. Accordingly, our results demonstrate that E inhibits the action of $PPAR{\gamma}$ on adipogenesis through E activated ER, providing evidence that lack of estrogen may potentiate $PPAR{\gamma}$ action on adipogenesis.

• 한국동물학회지
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• 제37권3호
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• pp.377-384
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• 1994

The present study examines the inhibitow effect of progesterone (P) on luteinizing hormone $(LH)\beta$ subunit gene expression in anterior pituitary of ovariectomized, estradiol-treated adult rats. A single injection of P (1mg) further decreased the estradiol-Induced decrease in $LH\beta$ mRNA levels in ovariectomTzed rats in a time-dependent manner. p suppressed UIP mRNA levels at lower doses (0.1 and 1mg), but increased $LH\beta$ mRNA levels 81 a high dose (toms). The inhibitor action of P on $Uf\beta$ mRNA was restored when Ru486, a P receptor antagonist, was administered 1h before P treatment. These data clearly indicate that P inhibits gene expression of $LH\beta$ in the rift pituitary in a swersic manner with estrogen.

• The Korean Journal of Physiology and Pharmacology
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• 제9권4호
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• pp.231-238
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• 2005

Neuronal apoptotic events, which result in cell death, are occurred in hypoxic/ischemic conditions. Estradiol is a female sex hormone with steroid structure known to provide neuroprotection through multiple mechanisms in the central nervous system. This study was aimed to investigate the signal transduction pathway of $CoCl_2$-induced neuronal cell death and the inhibitory effects of estradiol. Administration of $CoCl_2$ decreased cell viability in both a dose- and time-dependent manner in PC12 cells. $CoCl_2$-induced cell death produced genomic DNA fragmentation and morphologic changes such as cell shrinkage and condensed nuclei. It was found that $CoCl_2$-treated cells increased the reactive oxygen species (ROS) as well as caspase-8, -9 and -3 activities. However, pretreatment with estradiol before exposure to $CoCl_2$ prevented the reduction in cell viability reduction and attenuated DNA fragmentation and morphologic changes caused by $CoCl_2$. Furthermore, the $CoCl_2$-induced increases of ROS levels and caspases activities were attenuated by estradiol. Gene expression analysis revealed that estradiol blocked the underexpression of the Bcl-2 and ameliorated the increase in the release of cytochrome c from mitochondria into cytoplasm and Fas-ligand (Fas-L) upregulated by $CoCl_2$. These results suggest that $CoCl_2$ induce apoptosis in PC12 cells through both mitochondria- and death receptor-mediated cell death pathway. Estradiol was found to have a neuroprotective effect against $CoCl_2$-induced apoptosis through the inhibition of ROS production and by modulating apoptotic effectors associated with the mitochondria- and death-dependent pathway in PC12 cells.

• 한국발생생물학회지:발생과생식
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• 제6권2호
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• pp.123-129
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• 2002

비만유전자 산물인 leptin은 비만뿐만 아니라 여성의 생식 생리와 관련이 있는 것으로 보이나, 아직 이러한 leptin이 난소에 직접적으로 작용하는지 정확하게 밝혀지지 않고 있다. 따라서 본 연구에서는 흰쥐 난소에서 leptin과 leptin 수용체의 발현을 면역조직화학방법으로 확인하고 발정주기에 따른 leptin과 leptin 수용체의 발현 양상을 RT-PCR 방법으로 조사하고자 하였다. 면역조직화학적 염색방법 결과 흰쥐 난소내에서 leptin은 협막세포와 폐쇄 난포의 일부 과립세포에 염색되었고, leptin 수용체는 협막세포, 간질세포와 난포강이 형성되지 않은 난포의 난자에 염색되었다. 특히 폐쇄 난포에서는 leptin과 leptin 수용체가 정상 난포에 비해 강하게 염색되었다. 흰쥐의 발정주기 동안 혈청내 estradiol, progesterone leptin의 농도는 ELISA 방법으로 측정하였고, 난소내 leptin과 leptin 수용체의 mRNA 발현 양상은 RT-PCR 방법으로 조사하였다. 혈중 leptin 농도를 측정한 결과 estrous 시기에 비하여 metestrous 시기에 유의하게 증가하였고, 이 시기에 progesterone 농도가 함께 증가하는 것을 관찰할 수 있었다. Leptin mRNA는 모든 발정주기에서 발현되지 않았지만 leptin 수용체 mRNA는 diestrous 시기를 제외한 다른 발정주기에 모두 발현되었다. 이러한 결과는 leptin이 흰쥐 난소의 기능을 조절하는데 직접적으로 관여할 수 있다는 것을 제시하고 있다.

• Clinical and Experimental Reproductive Medicine
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• 제26권3호
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• pp.383-387
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• 1999

Objective: There is increasing evidence for the expression of rat in gene in several extrapituitary sites including testis and ovary. We also have demonstrated that the local LH expression in the rat epididymis and uterus, the major accessory sex organs in male and female reproductive system, respectively. Design: The present study was undertaken to elucidate whether the gene for LH receptor is expressed in rat uterus and whether the expressions of uterine LH and its receptor are differentially regulated during estrous cycle. Presence of the transcripts for rat LH receptor in the rat uterine tissue were confirmed by touchdown reverse transcription-polymerase chain reaction (RT-PCR). Results: In $LH{\beta}$ semi-quantitative RT-PCR, the highest expression level was shown in estrus stage. The level of ill receptor transcripts was also fluctuated during estrous cycle. In ovariectomized rats (OVX + Oil), the expressions of both uterine LH and LH-R were markedly reduced when compared to those from normal rats. Supplement with estradiol $17{\beta}$ to the ovariectomized rats (OVX + $E_2$) restored the expression levels of LH and its receptor to the levels in uteri from normal rats. Conclusion: Our findings indicated that 1) LH and its receptor gene are expressed in the rat uterus from cycling rats, 2) the expression of uterine LH and its receptor is mainly, if not all, under the control of ovarian sex steroid(s). These results suggested that the uterine LH may act as a local regulator with auto and/or paracrine manner, though the posibility that the pituitary LH may act directly on the regulation of uterine functions could not be discarded.

• 동의신경정신과학회지
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• 제18권1호
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• pp.15-36
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• 2007

Objective : This study was to investigate the effects of several herbs on the levels of MT1 and MT2 melatonin receptors Methods: It was investigated the effects of several herbs such as WEDL, WEZV, WEFO, WEOC on the levels of MT1 and MT2 melatonin receptors using C6 glial cell model. ${\beta}-estradiol$ treatment, as a positive control group, under non-cytotoxic condition. Results : 1. The water extracts of Dimocarpus long (WEDL) induced the levels of MT2 melatonin receptor expression in a concentration-dependent manner without altering the levels of MT1 melatonin receptor expression. 2. The treatment with the water extract of Zizyphus vulgaris (WEZV) induced the levels of MT1 melatonin receptor expression and the levels of MT2 melatonin receptor expression was not affected. 3. The levels of MT1 as well as MT2 melatonin receptor expression were markedly up-regulated in the water extract of Fossilia ossis (WEFO) and the water extract of Ostreae caro (WEOC)-treated C6 cells. 4. The combination treatment with WEDL and WEZV induced not only the levels of MT1 melatonin receptor expression but also MT2 melatonin receptor expression, but the synergic effects of the combination treatment with WEFO and WEOC were not detected in C6 cells. Conclusion : The study provides important new insights into the possible mechanisms on the regulation of melatonin receptor synthesis by WEDL, WEZV, WEFO and WEOC.

• Animal cells and systems
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• 제1권1호
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• pp.115-121
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• 1997

To precisely analyze the role of ovarian steroids in the regulation of laminin chain gene expression in mouse uterine tissues, the ovariectomized mouse model was used. Ovariectomized mice received a single injection of steroid hormones and total RNA was isolated from whole uterine tissues. Messenger RNA levels of each laminin chain (A, 81, and 82) were determined by competitive RT-peR procedures. Estradiol decreased mRNA levels of laminin 81 chain about two-fold, and 82 chain rather moderately. Estradiol-induced inhibition of laminin 81 and 82 chain mRNA levels were completely blocked by pretreatment with estrogen receptor antagonist tamoxifen. Estriol, a short acting estrogen which cannot induce hyperplastic responses of rodent uterine tissues, also showed an inhibitory effect on 81 and 82 chain mRNA levels, while estrone, an inactive estrogen, failed to influence either 8 chain mRNA levels. Effects of steroids on A chain mRNA level were quite different from those on 8 chains. Laminin A chain mRNA level was slightly increased by estradiol treatment, but negatively affected by progesterone. Progesterone treatment greatly increased both 8 chain mRNA levels, but slightly decreased A chain mRNA level compared to the control. The effect of progesterone on laminin chain-specific mRNA levels was further increased by co-injection of estradiol in a time-dependent manner. Progesterone-induced 81 and 82 chain mRNA transcription was inhibited by RU486, a synthetic anti-progesterone /anti-glucocorticoid. The present study demonstrates for the first time that steroids are able to regulate laminin gene expression in mouse uterine tissues, indicating that steroid-regulated laminin gene expression is involved in uterine growth and probably differentiation.

• Fisheries and Aquatic Sciences
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• 제24권10호
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• pp.330-339
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• 2021

Oyster (Crassostrea gigas) is a marine bivalve mollusk widely distributed in coastal areas, and have been long widely used in industrial resources. Several studies demonstrated that fermented oyster (FO) extract attribute to bone health, but whether administration of FO play as an endocrine disruptor has not been studied. Therefore, in the present study, we investigated the effect of FO on the endocrine system in vitro and in vivo. As the results of the competitive estrogen receptor (ER) and androgen receptor (AR) binding affinities, FO was not combined with ER-α, ER-β, and AR. However, 17β-estradiol and testosterone, used as positive control, were interacted with ER and AR, respectively. Meanwhile, oral administration of 100 mg/kg and 200 mg/kg of FO doesn't have any harmful effect on the body weight, androgen-dependent sex accessory organs, estrogen-dependent-sex accessory organs, kidney, and liver in immature rats. In addition, FO supplementation has no effect on the serum levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone, and 17β-estradiol. However, the relative weight of androgen- and estrogen-dependent organs were significantly increased by subcutaneously injection of 4.0 mg/kg of testosterone propionate (TP) and by orally administration of 1.0 ㎍ of 17α-ethynyl estradiol (EE) in immature male and female rats, respectively. Furthermore, TP and EE administration markedly decreased the serum LH and FSH levels, which are similar those of mature Sprague-Dawley (SD) rat. Furthermore, the testosterone and 17β-estradiol levels were significantly enhanced in TP and EE-treated immature rats. Taken together, our findings showed that FO does not interact with ER and AR, suggesting consequentially FO does not play as a ligand for ER and AR. Furthermore, oral administration of FO did not act as an endocrine disruptor including androgenic activity, estrogenic activity, and abnormal levels of sex hormone, indicating FO may ensure the safety on endocrine system to develop dietary supplement for bone health.

• 한국식품영양과학회지
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• 제33권9호
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• pp.1486-1491
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• 2004

식품오염 관련 중금속들의 에스트로겐성을 in vitro 와 in vivo 분석방법을 병행하여 평가하였다. 분석방법은 1) estrogen receptor dependent transcriptional expression 분석법, 2) E-screen assay 그리고, 3) 마우스 자궁비대시험 (uterotropic assay)을 사용하였다. 시험에 사용한 물질로는 $17\beta$-estradiol, diethylstilbestrol(DES), arsenic oxide, bis (tri-n-butyltin), cadmium chloride, chromium chloride, lead acetate, mercuric chloride을 사용하였다. Estrogen receptor dependent transcriptional expression 분석 결과, bis(tri-nbutyltin) > cadmium chloride > chromium chloride 순으로 에스트로겐성이 크게 나타났으며, mercuric chloride, lead acetate, arsenic oxide는 거의 나타나지 않았다. E-screen test 결과, bis(tri-n-butyltin) > cadmium chloride > chromium chloride 순으로 에스트로겐성이 크게 나타났으며, mercuric chloride, lead acetate, arsenic oxide는 거의 나타나지 않았다. 자궁비대시험 결과도 마찬가지로 bis(tri-nbutyltin), cadmium chloride, chromium chloride은 자궁중량 비대를 크게 초래하였으며, 반면에 mercuric chloride, lead acetate, arsenic oxide는 그러한 효과가 미약하거나 없었다. 세 분석방법 결과 bis(tri-n-butyltin), cadmium chloride, chromium chloride 순으로 에스트로겐성이 크게 나타났다. 이러한 결과는 최근 bis(tri-n-butyltin)과 cadmium chloride이 에스트로겐성이 있다는 다른 연구결과들과 잘 일치하며, 또한 크롬화합물도 에스트로겐성이 있다는 것을 새롭게 제시하고 있다. 본 연구는 세 단계 수준(전사활성화단계, 세포증식작용, in vivo assay)의 분석을 병행함으로써 수많은 중금속의 에스트로겐성을 효과적으로 평가할 수 있다는 것을 제시해주고 있다.

• Journal of Ginseng Research
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• 제12권2호
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• pp.104-113
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• 1988

여러가지 농도의 cholesterol을 함유한 배지에서 배양한 CHO 세포내로 흡입된 cholesterol 양을 조사한 결과 흡입량이 배지의 cholesterol 농도에 비례하였으므로 cholesterol 흡입은 확산에 의한 것으로 생각된다. $^{125}I$으로 표지된 저밀도 지방단백질($^{125}I$-LDL)을 이용하여 여러가지 농도의 cholesterol을 함유한 배지에서 배양한 CHO 세포와 cholesterol이 없는 정상배지에서 배양한 CHO 세포에서의 LDL 수용체의 합성양상을 조사한 결과 배지에 가해준 cholesterol이 LDL 수용체 합성을 억제함을 확인하였다. Cholesterol의 LDL 수용체 생합성 억제작용에 미치는 ginsenoside의 영향을 조사하기 위해 ginsenoside와 cholesterol을 함께 함유한 배지에서 배양한 CHO 세포(시험군)과 cholesterol만을 포함한 배지에서 배양한 CHO 세포(대조군)에서의 LDL 수용체의 활성양상을 분석한 결과 대조군에 비해 시험군에서의 LDL 수용체 활성이 크게 증가하였다. RNA 및 단백질 합성도 시험군이 대조군보다 증가하였음을 관찰하였다. 그러나 이와 같은 실험조건하에서의 대조군과 시험군의 cholesterol농도를 측정한 결과 시험군의 cholesterol 농도가 대조군보다 훨씬 저하되고 있었다. Ginsenoside의 cholesterol농도 저하작용을 관찰하기 위해 CHO세포에서의 cholesterol의 steroid hormone(estradiol, progesterone)으로의 전환에 미치는 ginsenoside의 영향을 조사한 결과 ginsenoside는 cholesterol의 hormone으로의 전환을 촉진하였음이 확인되었다. 위와 같은 실험결과로 볼 때 ginsenoside는 CHO 세포내부에서의 cholesterol의 LDL 수용체 합성억제를 완화시켜 주는 것이라고 생각된다.