• Journal of Periodontal and Implant Science
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• v.32 no.3
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• pp.445-456
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• 2002

The purpose of this study were to determine that dexamethasone(Dex) induces differentiation of periodontal ligament(PDL) cells to osteoblastic cells and to investigate expression of matrix Gla protein(MGP), which is one of bone matrix protein. The isolated human PDL cells and gingival fibroblasts were prepared and cultured. The fourth or sixth sub-passage cells were used in this experiments. control group, ascorbic acid and ${\beta}$-glycerophosphate treated group, ascorbic acid, ${\beta}$-glycerophosphate and l00nM Dex treated group, ascorbic acid, ${\beta}$-glycerophosphate, and 5 ${\mu}M$ Dex treated group were made for study. The results were as follows: Cellular morphological change of PDL cells according to time was investigated. At first, the cells exhibited confluent monolayer of spindle or polygonal appearance. The multilayer of cells were seen after 7 days of treatment. After 14 days, the cells lost polarity and were densely packed. The mineralized nodule formation was seen at 21 days in the only Dex treated PDL cell groups. In the gingival fibroblast groups and no Dex treated PDL cell groups, the mineralized nodule was not seen. The mineralized nodule formation of 5 ${\mu}M$ Dex treated group was higher than 100 nM Dex treated group. Alkaline phosphatase(ALP) activity was higher in the Dex treated PDL cell groups of 14 and 21 days than 0 and 7 days. MGP was expressed in the control and all experimental groups and the expression was constant at 0,7,14,21 day. The above results confirm that Dex is affected to differentiation of the PDL cells to osteoblastic or cementoblastic cells and has dose-dependent effect for mineralization. And, MGP is expressed in the PDL cells and is not affected to mineralization of PDL cells.

• Journal of Microbiology and Biotechnology
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• v.33 no.7
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• pp.915-925
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• 2023

Sarcopenia is defined as loss of muscle mass and strength due to aging. Recent studies show that sarcopenia may improve via the gut-muscle axis, suggesting that gut health may affect muscle phenotypes. In this study, we aimed to investigate the ability of Lactobacillus rhamnosus JY02 as a probiotic strain isolated from kimchi to alleviate sarcopenia. L. rhamnosus JY02-conditioned medium (CM) reduced dexamethasone (DEX)-induced myotube diameter atrophy and expression of muscle degradation markers (MuRF1 and atrogin-1) in C2C12 cells. The amelioration of sarcopenia was investigated by measuring body composition (lean mass), hand grip strength, myofibril size (using histological analysis), and mRNA and protein expression of muscle-related factors in a DEX-induced mouse model. The results of these analyses showed that L. rhamnosus JY02 supplementation promoted the production of muscle-enhancement markers (MHC Iβ, MHC IIα, and Myo-D) and reduced both the production of muscle degradation markers and the symptoms of muscle atrophy (loss of lean mass and muscle strength). We also found decreased levels of pro-inflammatory cytokines (IL-6, IFN- γ) and increased levels of anti-inflammatory cytokines (IL-10) in the serum of DEX+JY02-administered mice compared to those in DEX-treated mice. Overall, these results suggest that L. rhamnosus JY02 is a potent probiotic supplement that prevents sarcopenia by suppressing muscle atrophy.

• Journal of Pharmaceutical Investigation
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• v.41 no.5
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• pp.279-288
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• 2011

The Dexamethasone (DEX) loaded chitosan microspheres were prepared by thermal denaturation and chemical cross-linking method using a dierent concentration of glutaraldehyde as chemical cross-linking agent. The prepared microspheres were evaluated for the percentage of Drug Loading (DL), Encapsulation Efficiency (EE) and surface morphology by Scanning Electron Microscopy (SEM). DL and EE were found to be maximum range of 10.0 to 10.79 % and 58.19 to 64.73 % respectively. The SEM Photographs of the resultant microspheres exhibited fairly smooth surfaces and predominantly spherical in appearance. In addition, Fourier Transform Infrared Spectroscopy (FTIR) and Differential Scanning Calorimetry (DSC) shown that there was no interaction between the drug and polymer. In vitro and in vivo release studies revealed that the release of dexamethasone was sustained and extended up to 63 days and effectively controlled by the extent of cross-linking agent. Non-clinical parameters such as paw volume, hematological parameters like Erythrocyte Sedimentation Rate (ESR), Paced Cell Volume (PCV), Total Leucocytes Count (TLC), Hemoglobin (Hb), Differential Cell Count (DCC) were investigated in Fruend's Complete Adjuvant (FCA) induced arthritic rats. Radiology and histopathological studies were also performed in order to evaluate the therapeutic efficacy of the DEX-loaded microspheres in extenuating the rat arthritic model.

• Journal of Periodontal and Implant Science
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• v.33 no.4
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• pp.573-584
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• 2003

Bone remodeling results from the combined process of bone resorption and new bone formation which is regulated in part by some of Dexamethasone related proliferation & mineralization of cultured bone cell and polypeptide growth factors such as platelet derived growth factor(PDGF), which has been known to be an important local regulator of bone cell activity and participate in normal bone remodeling. To evaluate the effects of Dex and PDGF on bony healing of calvarial defect in rats, 10 ng/ml PDGF were applied on P group and 10 ng/ml PDGF and $10^7$ M Dex were applied PD group. 4 rats in each group were sacrificed at 7, 14. 21 days after operation respectively, and the tissue blocks were prepared for light microscope with H-E for evaluation of overall healing, with TRAP(tartrate resistant acid phosphatase) for evaluation of osteoclastic activity and with immunohistochemical staining for macrophages. The results were as follows : 1. In all group, healing aspects were progressed from 7 days to 21 days in soft and bony tissue, but complete repair were not observed in bony defect 2. PDGF and control group were showed similar bony healing aspect , but bony healing in combination of PDGF-BB and Dex were observed slower aspect compared to PDGF and control group from early healing times. 3. There were no significant difference on activities of osteoclast and macrophages in bony healing between control and experimental group In conclusion, PDGF were not influenced on bony healing of defect and combination of PDGF-BB and Dex were showed slower healing through early healing times. it was considered that Dex compared to PDGF did influenced on early hone formation factors in healing period

• Journal of Periodontal and Implant Science
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• v.29 no.2
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• pp.277-289
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• 1999

The ultimate aim of periodontal treatment is periodontal regeneration, which necessiates the regeneration of bone tissues. To evaluate the effects of Dex growth and differentiation of MC3T3-E1 cells, cells were seeded in alpha-modified eagle medium containing 10% fetal bovine serum, 10mM beta-glycerophosphate , $50{\mu}g/ml$ of ascorbic acid, with or without $10^{-7}M$ Dex and examined cell proliferation activities, alkaline phosphatase activities, and bone nodule formation until 25days. The results were as follows : 1. In Dex group, cell proliferation activities were lower until 15 days compared to control group. Bone nodules formation were showed at 10 days. 2. In the time-response effect, ALP activities were increased until the 10 days in control groups thereafter decreased and ALP activities of Dex group were lower aspect than control group until the 10 days In this study, bone nodule formation of osteoblast-like cells were accelerated by Dex and cell proliferation activities, ALP activity of Dex group showed lower than control group. Dex was considered that it did suppress initial growth, but accerelate mineralization of osteoblast-like cells.

• IMMUNE NETWORK
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• v.7 no.1
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• pp.18-25
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• 2007

Background: Although glucocorticoids (GCs) are effective in controlling asthma in the majority of patients, a subset of asthmatics fails to demonstrate a satisfactory response, even to systemic GC therapy. This population is referred to as being "steroid-resistant". The actual mechanism underlying steroid resistance in asthma remains to be elucidated. Methods: We have investigated how dexamethasone (DEX) regulates asthmatic phenotypes in a murine model of asthma, in which mice received i.p. immunization twice, followed by two bronchoprovocations with aerosolized OVA with a one-week interval, which we have recently described. Results: Pretreatment with DEX resulted in an inhibition of NF-${\kappa}B$ activation in asthmatic lungs, and also inhibited bronchoalveolar lavage (BAL) levels of NF-${\kappa}B$-dependent cytokines such as TNF-${\alpha}$ and CC chemokines [eotaxin and monocyte chemotactic protein (MCP)-1]. DEX was effective in suppressing airway hyperresponsiveness (AHR) at 10 h, Th2-dependent asthmatic phenotypes such as airway eosinophilia, BAL levels of Th2 cytokines (IL-5 and IL-13), and mucin production. However, DEX failed to suppress BAL levels of CXC chemokines [macrophage inflammatory protein-2 (MIP-2) and keratinocyte-derived chemokine (KC)] and airway neutrophilia. Conclusion: Airway neutrophilia is among the phenomena observed in patients with severe GC-resistant asthma. This study will provide insight into the molecular basis for airway neutrophila seen in steroid-resistant asthma. Further studies are required to delineate the underlying mechanism of CXC chemokine expression in asthma.

• IMMUNE NETWORK
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• v.22 no.4
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• pp.33.1-33.17
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• 2022

Suppressors of cytokine signaling (SOCS) have emerged as potential regulators of macrophage function. We have investigated mechanisms of SOCS3 action on type 2 macrophage (M2) differentiation induced by glucocorticoid using human monocytic cell lines and mouse bone marrow-derived macrophages. Treatment of THP1 monocytic cells with dexamethasone (Dex) induced ROS generation and M2 polarization promoting IL-10 and TGF-β production, while suppressing IL-1β, TNF-α and IL-6 production. SOCS3 over-expression reduced, whereas SOCS3 ablation enhanced IL-10 and TGF-β induction with concomitant regulation of ROS. As a mediator of M2 differentiation, glucocorticoid-induced leucine zipper (GILZ) was down-regulated by SOCS3 and up-regulated by shSOCS3. The induction of GILZ and IL-10 by Dex was dependent on ROS and p38 MAPK activity. Importantly, GILZ ablation led to the inhibition of ROS generation and anti-inflammatory cytokine induction by Dex. Moreover, GILZ knock-down negated the up-regulation of IL-10 production induced by shSOCS3 transduction. Our data suggest that SOCS3 targets ROS- and p38-dependent GILZ expression to suppress Dex-induced M2 polarization.

• Korean Journal of Veterinary Research
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• v.35 no.2
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• pp.337-345
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• 1995

To evaluate the pathogenicity and immunogenicity of Eimeria tenella to the chicken treated with dexamethasone(DEX) and testosterone propionate (TES), we administered 0.1ml/chicken of dexamethasone and 40mg/chicken of testosterone propionate at 1-, 2-, and 7-days old, respectively. We also immunized with ND oil-emulsion vaccine at 2 weeks old. After that, we immunized and challenged with 100 and $1{\times}10^5$ oocysts/chicken of E tenella at 2 and 4 weeks old, respectively. And then we investigated the HI titers for ND virus, survival rate, body weight gain, lesion score and the weight of the bursa of Fabricius and thymus. The titers for ND virus in the groups treated with TES were higher than those in the groups treated with DEX and CON during 3 to 6 weeks. After challenge, the survival rate of testosterone propionate treated-challenged(TES-CHA) and TES-immunized and challenged(TES-V&C) groups were 61.5 and 83.3% and those of the other groups were all 100%. At 1 week after challenge, the lesion scores of TES-CHA group(4.0) was the highest of all experimental groups. Those of DEX and controlchallenged( CON-CHA) groups were 2.8, and those of all V&C groups were 2.4. During 1 and 2 weeks after immunization, the body weight gains of TES groups were severe low(61.6-82.2g and 189.6-260.4g). During 1 and 2 weeks after challenge, the body weight gains of all CHA groups were lower than those of not challenged groups. But, those of all V AC groups were not different from those of not immunized groups. At 4- and 6-weeks old, the weight of the bursa of Fabricius and thymus in the chicken of all TES groups were lower than those of all control (CON) and DEX groups. Therefore, testosterone propionate acted as immunosuppressive drug. Also, it was thought that the chicken affected a little humoral immunity to E tenella.

• Journal of Food Hygiene and Safety
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• v.38 no.2
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• pp.69-78
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• 2023

This study aimed to investigate the protective effect of enzymatically modified stevia (EMS) on C2C12 cell-based model of dexamethasone (DEX)-induced muscle atrophy to provide baseline data for utilizing EMS in functional health products. C2C12 cells with DEX-induced muscle atrophy were treated with EMS (10, 50, and 100 ㎍/mL) for 24 h. C2C12 cells were treated with EMS and DEX to test their effects on cell viability and myotube formation (myotube diameter and fusion index), and analyze the expression of muscle strengthening or degrading protein markers. Schisandra chinensis Extract, a common functional ingredient, was used as a positive control. EMS did not show any cytotoxic effect at all treatment concentrations. Moreover, it exerted protective effects on C2C12 cell-based model of DEX-induced muscle atrophy at all concentrations. In addition, the positive effect of EMS on myotube formation was confirmed based on the measurement and comparison of the fusion index and myotube diameter when compared with myotubes treated with DEX alone. EMS treatment reduced the expression of muscle cell degradation-related proteins Fbx32 and MuRF1, and increased the expression of muscle strengthening and synthesis related proteins SIRT1 and pAkt/Akt. Thus, EMS is a potential ingredient for developing functional health foods and should be further evaluated in preclinical models.

• Preventive Nutrition and Food Science
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• v.9 no.4
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• pp.336-341
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• 2004

Leptin, resisitn and PAI-1 (plasminogen activator inhibitor-1) are synthesized and secreted by rodent fat cells and recently postulated to be an important link to obesity. This study was conducted to characterize the hormonal regulation of leptin, resistin, and PAI-1 gene expression in the 3T3-L1 adipocytes. The cells were treated with 0.5 $\mu$M insulin, 1 $\mu$M dexamethasone (Dex), or 0.05 $\mu$M triiodothyronine (T3) for 72 hours. The mRNA levels of each peptide were measured by semi-quantitative RT-PCR. The mRNA level of the leptin-producing ob gene was significantly increased by insulin, Dex, and T3 by 3.2-, 3.1- and 2.7-fold, respectively, compared to the control (p < 0.05). The level of resistin mRNA was increased by insulin, Dex, and T3 by 2.7-, 2.5- and 2-fold, respectively, compared to the control (p < 0.05). Likewise, the level of PAI-1 mRNA was significantly increased by insulin, Dex, and T3 compared to the control (p < 0.05). Taken together, our results suggest that insulin, Dex, and T3 may regulate the gene expression of leptin, resistin, and PAI-1 in 3T3-L1 adipocytes.