• Journal of Korean Academy of Oral and Maxillofacial Radiology
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• v.19 no.1
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• pp.69-87
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• 1989

It is well known that the glucocorticoid induces osteoporosis by suppression of the osteoblast, but its effect on the osteoclast hRS some controversy whether it activates or suppresses the osteoclast. If the calcitonin, which is known to suppress the osteoclast, prevents the osteoporosis by glucocorticoid, then the suppression of the osteoclast by the glucocorticoid is not so significant. And if the calcitonin increases the osteoblastic activity, Tc-99m MDP uptake will be increased in spite of the glucocorticoid effect on the osteoblast. The immobilization operation was performed to the right leg of male Wistar rats weighing about 200gm. each. For 16 weeks after operation, rats were injected glucocorticoid alone or glucocorticoid anci calcitonin. The bone density was measured by means of photodensitometry under reference aluminum step wedge and Tc-99m MDP uptake was available to the index of the osteoblastic activity. 1. The bone density of femora! head was markedly reduced than that of femoral shaft following ration of cancellous and cortical components in both site. 2. Glucocorticoid caused decrease in bone density of spine and femur, md there is significantly increase of it when medication of glucocorticoid and calcitonin injection simultaneously than that of glucocorticoid. 3. Tc-99m MDP uptake was revealed significant reduction in medication of glucocorticoid but increase in gi;.:cocorticoid and calcitonin injection simultaneously in later experimental period. 4. There wail, a slight reduction in plasma osteocalcin in medication of glucocorticoid through experimental periods and an increase in its value in case of giving glucocorticoid and calcitonin simultaneously in later experimental period. From these results, we suggest that osteoporosis by immobilization is more pronounced by glucocorticoid hormone and osteoporosis induced by immobilization and glucocorticoid use is prevented by calcitonin administration with increasing osteoblastic activity.

• BMB Reports
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• v.42 no.7
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• pp.421-426
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• 2009

Glucocorticoids regulate multiple physiological processes such as metabolic homeostasis and immune response. Mouse Pon2 (mPon2) acts as an antioxidant to reduce cellular oxidative stress in cells. In this present study, we investigated the transcriptional regulation of mPon2 by glucocorticoids. In the presence of glucocorticoid analogue dexamethasone, the expression of mPon2 mRNA in cells was increased, whereas the expression was inhibited by a transcription inhibitor actinomycin D. Glucocorticoid receptors bound to the putative glucocorticoid response elements located between -593 bp and -575 bp of the mPon2 promoter. Transcriptional activity was completely blocked when the putative element was mutated. Taken together, these results suggest that the expression of the mPon2 gene is directly regulated by glucocorticoid-glucocorticoid receptor complexes.

• Journal of Marine Bioscience and Biotechnology
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• v.2 no.2
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• pp.81-85
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• 2007

Glucocorticoid hormone regulates numerous physiological processes, such as regulation of metabolism, and anti-inflammatory and immunosuppressive actions via the activation and repression of gene expression. Here we described a lentivirus-based reporter vector system expressing red fluorescent protein (mRFP) or firefly luciferase (Luc) under the control of a glucocorticoid-responsive element that allows observation of the temporospatial pattern of glucocorticoid induced GR-mediated signaling on a cellular level. Moreover, usage of the chromatin insulator of the chicken ${\beta}$-globin locus induced a marked increase of sensitivity of glucocorticoid inducible promoter of a reporter gene. Use of this method will be applicable of screening for agonist and antagonist of GR in vitro, and also a reporter gene assay for the in vivo determination of the GR-mediated gene activation.

• Bulletin of the Korean Chemical Society
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• v.26 no.8
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• pp.1209-1213
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• 2005

Nuclear membrane is one of the main barriers in intracellular delivery of genetic materials. The previous report showed that glucocorticoid receptor dilated the nuclear pore to 60 nm in the presence of a ligand. It was also suggested that the transport of genetic material to nucleus might be facilitated by glucocorticoid. In this study, the effect of glucocorticoid preincubation in the polymeric gene delivery was investigated. The cells were preincubated with dexamethasone, a potent glucocorticoid, and transfection assays were performed with polyethylenimine (PEI) and polyamidoamine (PAMAM) dendrimer. As a result, the transfection efficiency of PEI or PAMAM to the cells in the presence of dexamethasone was enhanced, compared to the cells without dexamethasone. This effect was not observed in the cells preincubated with cholesterol. The polymer/DNA complex was stable in the presence of dexamethasone. In addition, the cytotoxicities of the polymeric carriers to the cells were observed in the presence of dexamethasone. In conclusion, dexamethasone enhances the transfection efficiency of polymeric carriers and may be useful in the development of polymeric gene carriers.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.4
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• pp.995-1000
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• 2004

This study was purposed to investigate the effect of Gamgung-tang(GGT) on immune responses induced by glucocorticoid in mice. GGT solution was treated by intraperitoneal injection for 7 days after glucocorticoid treatment(80㎎/㎏). And then B and T cell proliferation and cytolytic activity of natural killer(NK) cells were measured. There was 25% inhibition in B cell proliferation with treatment of glucocorticoid. However, B cell proliferation was not influenced by GGT treatment. T cell proliferation was also inhibited by 18.4% with treatment of glucocorticoid. On the other hand, T cell proliferation was increased dose-dependent manner in GGT treated group. Furthermore in purified T cell, the proliferation was furtherly increased than non-purified T cell. At concentration of 18㎎/mouse GGT, purified T cell proliferation was increase to above level of normal group. The cytotoxic activity of NK cell was decreased by 35.3% with treatment of glucocorticoid. In GGT treated group, the cytotoxic activity of NK cell was increased to the normal level. In purified NK cell, the cytolytic activity of NK cell was further increased than non-purifed NK cell. These results suggest that GGT may proliferate T cell that is suppressed by glucocorticoid, and activate NK cell activity.

• Molecules and Cells
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• v.39 no.8
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• pp.631-638
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• 2016

Glutathione peroxidase 3 (GPx3), an antioxidant enzyme, acts as a modulator of redox signaling, has immunomodulatory function, and catalyzes the detoxification of reactive oxygen species (ROS). GPx3 has been identified as a tumor suppressor in many cancers. Although hyper-methylation of the GPx3 promoter has been shown to down-regulate its expression, other mechanisms by which GPx3 expression is regulated have not been reported. The aim of this study was to further elucidate the mechanisms of GPx3 regulation. GPx3 gene analysis predicted the presence of ten glucocorticoid response elements (GREs) on the GPx3 gene. This result prompted us to investigate whether GPx3 expression is regulated by the glucocorticoid receptor (GR), which is implicated in tumor response to chemotherapy. The corticosteroid dexamethasone (Dex) was used to examine the possible relationship between GR and GPx3 expression. Dex significantly induced GPx3 expression in H1299, H1650, and H1975 cell lines, which exhibit low levels of GPx3 expression under normal conditions. The results of EMSA and ChIP-PCR suggest that GR binds directly to GRE 6 and 7, both of which are located near the GPx3 promoter. Assessment of GPx3 transcription efficiency using a luciferase reporter system showed that blocking formation of the GR-GRE complexes reduced luciferase activity by 7-8-fold. Suppression of GR expression by siRNA transfection also induced down-regulation of GPx3. These data indicate that GPx3 expression can be regulated independently via epigenetic or GR-mediated mechanisms in lung cancer cells, and suggest that GPx3 could potentiate glucocorticoid (GC)-mediated anti-infla-mmatory signaling in lung cancer cells.

• The Korean Journal of Zoology
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• v.38 no.3
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• pp.426-432
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• 1995

Expression of $\beta$-lactoglobulin gene in mammary tissue is strongly induced by lactogenic hormones such as prolactin, glucocorticoid, and insulin. In order to elucidate the regulatory mechanism underlying such hormonal induction, the response of the caprine $\beta$-lactoglobulin gene promoter to lactogenic hormones was analyzed in cultured HC11 mammary cells. Expression with serial deletions of the 5' -regulatory sequence of the $\beta$-lactoglobulin promoter revealed that two regions are responsible for a substantial change in hormonal indudbility. The region upstream of-1692, which exhibited strong repression of the downstream promoter, mediated the induction by insulin. This insulin-response was independent of the other two lactogenic hormones, prolactin and glucocorticoid. The other region from -740 to -470, which showed strong activation of the $\beta$-lactoglobulin promoter in confluent HC11 mammary cells, mediated mainly the response to a glucocorticoid analogue, dexametasone. The induction by the latter region, however, was suppressed by the usptream repression without insulin treatment. These results suggest that the induction of $\beta$-lactoglobulin promoter activity by lactogenic hormones in mammary cells may be achieved by the combined action of derepression by in sulin and activation by glucocorticoid and prolactin. Dexametasone response by the latter region seems to be mediated by the glucocorticoid receptor site around -7OObp.

• BMB Reports
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• v.48 no.7
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• pp.367-368
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• 2015

It has long been thought that glucocorticoid receptor (GR) functions as a DNA-binding transcription factor in response to its ligand (a glucocorticoid) and thus regulates various cellular and physiological processes. It is also known that GR can bind not only to DNA but also to mRNA; this observation points to the possible role of GR in mRNA metabolism. Recent data revealed a molecular mechanism by which binding of GR to target mRNA elicits rapid mRNA degradation. GR binds to specific RNA sequences regardless of the presence of a ligand. In the presence of a ligand, however, the mRNA-associated GR can recruit PNRC2 and UPF1, both of which are specific factors involved in nonsense-mediated mRNA decay (NMD). PNRC2 then recruits the decapping complex, consequently promoting mRNA degradation. This mode of mRNA decay is termed "GR-mediated mRNA decay" (GMD). Further research demonstrated that GMD plays a critical role in chemotaxis of immune cells by targeting CCL2 mRNA. All these observations provide molecular insights into a previously unappreciated function of GR in posttranscriptional regulation of gene expression. [BMB Reports 2015; 48(7): 367-368]

• The Journal of Korean Medicine
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• v.18 no.1
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• pp.326-336
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• 1997

In order to investigate the effect of aqua-acupuncture solution with Panax Ginseng into $Qihai(CV_6)$ and $Shenshu(BL_{23})$ on immune response induced by glucocorticoid in mouse, Panax Ginseng aqua-acupuncture solution was injected into $Qihai(CV_6)$ and $Shenshu(BL_{23})$ for seven days after injection with glucocorticoid. And then MA-HRP (methamphetamine-horseradish peroxidase) induced antibody production, numbers and lysozyme activity in macrophage were measured. The results were as follows: 1. The antibody production in mouse immunized with MA-HRP was decreased in control group as compared with normal group. Although $Qihai(CV_6)$ group showed slight increasement, $Shenshu(BL_{23})$ group indicated great increasement compared with normal group. However in Aa-BL group, antibody production was almost increased to normal group. 2. In control group, the numbers of macrophage were decreased about 14% as compared with normal group. And in the pretreated groups of $Qihai(CV_6)$ and $Shenshu(BL_{23})$ were respectively increased 3.0 times and 2.9 times as compared with normal group. 3. Effect of Panax Ginseng-aqua acupuncture solution on the lysozyme activity in macrophage was increased gradually in the pretreated groups of $Qihai(CV_6)$ and $Shenshu(BL_{23})$ as compared with control group. These results suggest that Panax Ginseng aqua-acupuncture at $Qihai(CV_6)$ and $Shenshu(BL_{23})$ may increase antibody production and lysozyme activity in macrophage that is suppressed by glucocorticoid, and Panax Ginseng aqua-acupuncture will have immuno adjuvant effects on the cells which concerned with immunomechanisms.

• Bulletin of the Korean Chemical Society
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• v.33 no.7
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• pp.2365-2368
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• 2012

The $11{\beta}$-hydroxysteroid dehydrogenase type 1 ($11{\beta}$-HSD1) enzyme is involved in modulation of glucocorticoid activity within target tissues. This enzyme may contribute to obesity and/or metabolic disease through its action in adipose or liver tissue. Inhibition of $11{\beta}$-HSD1 has major therapeutic potential for glucocorticoid-associated diseases, including obesity, diabetes (wound healing), and muscle atrophy. To develop such therapeutics, we performed a pharmacophore-based virtual screening (VS) for identification of novel $11{\beta}$-HSD1 inhibitors and found that the VS hit compounds show potent inhibition of $11{\beta}$-HSD1 enzyme activity. Further, we present a binding model for active compounds. The proposed pharmacophore may serve as a useful guideline for future design of new chemical entities as $11{\beta}$-HSD1-targeted antidiabetic agents.