• Journal of Korean Academy of Nursing
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• v.32 no.5
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• pp.727-734
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• 2002

This study was to determine the effect of DHEA administration before, during, and after dexamethasone treatment on body weight and TypeI,II muscle weight of rat receiving dexamethasone treatment. Method: Wistar rats were divided into 6 groups: control(C), dexamethasone(D), DHEA administration for 3days after dexamethasone treatment for 7days(7D+3DH), dexamethasone treatment for 7days after DHEA administration for 3days(3DH+7D), DHEA administration during dexamethasone treatment for 4days after dexamethasone treatment for 3days(3D+4DDH), DHEA administration during dexamethasone treatment for 7days(7DDH). Dexamethasone was injected by subcutaneously daily at a dose of 5mg/kg. DHEA was orally administered daily at a dose of 5mg/kg for 7 days. Soleus(TypeI) muscle, and both plantaris and gastro- cnemius(TypeII) muscles were dissected on the 7th day of experiment. Result: Body weight of both 3DH+7D group and 3D+4DDH group increased significantly compared with that of 7D group. Body weight of 7D+3DH group decreased significantly compared with that of 7D group, 7DDH group, 3DH+7D group and 3D+4DDH group. Muscle weight of both plantaris and gastro- cnemius tended to decrease compared with that of 7D group. Muscle weight of 7DDH group, 3D+4DDH group and 3DH+7D group increased significantly compared with that of 7D+3DH group. Muscle weight of gastrocnemius of both 3DH+7D group and 3D+4DDH group increased significantly compared with that of 7D group. Conclusion: Based on these results, it can be suggested that DHEA administration before and during dexamethasone treatment can increase both body weight and mass of atrophied TypeII muscle induced by dexa- methasone treatment.

• Journal of Korean Biological Nursing Science
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• v.3 no.1
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• pp.63-74
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• 2001

The purpose of this study was to determine the effect of DHEA with dexamethasone on body weight and wet weight and relative weight of atrophied hindlimb muscles induced by dexamethasone treatment. $200{\sim}225g$ Wistar rats were divided into control(C), dexamethasone(D), dexamethasone and DHEA(DDH) groups. Dexamethasone was injected daily at a dose of 5mg/kg. DHEA was administered daily at a dose of 5mg/kg by oral ingestion during 7days. The data were analyzed by Kruskal-Wallis test and Mann-Whitney U test using the SPSSWIN 9.0 program. Body weight and muscle weight of plantaris and gastrocnemius of dexamethasone group decreased significantly compared with that of control group. Muscle weight of plantaris of DDH group increased significantly compared with dexamethasone group. Body weight of DDH group decreased significantly compared to control group, but relative weight of plantaris and gastrocnemius of DDH group increased significantly compared to control group. Based on these results, it can be suggested that DHEA administration during dexamethasone treatment can be suggested that DHEA administration during dexamethasone treatment can increase weight of atrophied plantaris muscle induced by dexamethasone treatment.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.76-76
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• 2003

Mast cells accumulation can be causally related with several allergic inflammations. Previous work has demonstrated that glucocorticoids decreased tissue mast cell number and stem cell factor (SCF)-induced migration of mast cells required p38 mitogen-activated protein kinase (MAPK) activation. In the present study, we investigated the effects of dexamethasone on SCF-induced migration of rat peritoneal mast cells (RPMCs). SCF significantly induced migration of RPMCs at 4 h. Dexamethasone dose-dependently inhibited SCF-induced migration of RPMCs (about 90.1% at 100 nM, P<0.05). MAPK p38 inhibitor, SB203580 (20 ${\mu}$M) also inhibited the SCF-induced migration. The ability of SCF to enhance morphological alteration and F -actin formation was also abolished by treatment of dexamethasone. Dexamethasone inhibited SCF-induced p38 MAPK activation to near basal level and induced the MKP-1 expression. In addition, SCF-induced inflammatory cytokine production was significantly inhibited by treatment of dexamethasone or SB203580 (p<0.01). Our results show that dexamethasone potently regulates SCF -induced migration, p38 MAPK activation and inflammatory cytokine production through expression of MKP-l protein in RPMCs. Such modulation may have functional consequences during dexamethasone treatment, especially mast cell-mediated allergic inflammation disorders.

• Herbal Formula Science
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• v.28 no.1
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• pp.29-39
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• 2020

Objectives : Glucoraphanin is one of the well-known natural glucosinolates found in cruciferous plants. In the present study, we investigated the effects and molecular mechanism of glucoraphanin in dexamethasone-induced skeletal muscle atrophy in vitro model. Methods : The cytotoxic effects of glucoraphanin on C2C12 myoblasts or myotubes were evaluated by MTT assay. The glucoraphanin was evaluated effects in dexamethasone-induced skeletal muscle atrophy in C2C12 myotubes using a real-time PCR, western blots analysis, and immunofluorescence staining of myosin heavy chain. Result : Glucoraphanin had no cytotoxicity on both C2C12 myoblasts or myotubes. Dexamethasone markedly induced muscle atrophy by up-regulating muscle-specific ubiquitin E3 ligase markers, atrogin-1 and MuRF1, and down-regulating MyoD, a myogenic regulatory factor whereas co-treatment of glucoraphanin and dexamethasone dose-dependently inhibited it. Furthermore, decreased expressions of p-Akt, p-FOXO1, and p-FOXO3a induced by dexamethasone were reversed by co-treatment with glucoraphanin and dexamethasone. In addition, dexamethasone obviously reduced myotube diameters, while co-treatment of glucoraphanin and dexamethasone increased those to a similar level as control. Conclusions : These results show that glucoraphanin suppresses dexamethasone-induced muscle atrophy in C2C12 myotubes through activation of Akt/FOXO signaling pathway.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.6
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• pp.363-369
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• 2005

It is imperative to analyse brain injuries directly in real time, so as to find effective therapeutic compounds to protect brain injuries by stress. We established a system which could elucidate the real time $Ca^{2+}$ dynamics in an organotypic cultured hippocampal slice by the insults of artificial stress hormone, dexamethasone. The real time $Ca^{2+}$ dynamics could continuously be detected in cornus ammonis 3 (CA3) of the organotypic hippocampus for 8 hours under confocal microscopy. When dexamethasone concentration was increased, the $Ca^{2+}$ was also increased in a dose dependent manner at $1{\sim}100{\mu}M$ concentrations. Moreover, when the organotypic cultured hippocampal slice was treated with a glutamate receptor antagonist together with dexamethasone, the real time $Ca^{2+}$ dynamics were decreased. Furthermore, we confirmed by PI uptake study that glutamate receptor antagonist reduced the hippocampal tissue damage caused by dexamethasone treatment. Therefore, our new calcium ion dynamics system in organotypic cultured hippocampal slice after dexamethasone treatment could provide real time analysis method for investigation of brain injuries by stress.

• Herbal Formula Science
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• v.29 no.1
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• pp.45-55
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• 2021

Objectives : This study was conducted to evaluate the anti-atrophic effect of polycan in dexamethasone-induced skeletal muscle atrophy in vitro model. Methods : C2C12 myoblast were differentiated into myotube by 2% horese serum medium for 6 days, and then treated polycan extract at different concentrations for 24h. The effect of dexamethasone on the induction of muscle atrophy and expression of atrophy-related genes in differentiated C2C12 myotubes using a GSH, ROS, real-time PCR, western blots analysis. Results : The results showed that Treatment with polycan (100 and 200 ㎍/㎖) noncytotoxic levels on both myoblast and myotube. Polycan decreased the ROS level overproduced with dexamethasone and improved the depletion of GSH level. Dexamethasone showed a decrease in myotube diameter, which was associated with up-regulation muscle-specific ubiquitin ligases markers, such as atrogin-1, FoxO3, myostatin and muscle RING finger-1 (MuRF1), and down-regulation of myogenin, MEF2, Myogenic regulatory factor 5, 6 and MyoD. The results showed that polycan treatment significantly dose-dependently inhibited it. Furthermore, decreased expressions of PI3K/Akt signal pathway by dexamethasone were reversed by treatment with polycan. Conclusions : Thus, polycan suppresses dexamethasone induced muscle atrophy in C2C12 myotube in vitro model through activation of PI3K/Akt pathway and protective effect of improve skeletal muscle function.

• Journal of Korean Academy of Nursing
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• v.32 no.4
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• pp.550-559
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• 2002

This study was conducted to determine whether low intensity regular exercise following dexamethasone treatment could attenuate steroid-induced muscle atrophy. Method: 36 Wistar-rats(90-110g) were divided into six groups: control group(C), dexamethasone treatment group(D), sedentary group after normal sedentary period(C+S), sedentary group after dexamethasone treatment period(D+S), exercise group after normal sedentary period(C+E), and excercise group after dexamethasone treatment period(D+E). D, D+S, and D+E groups received dexamethasone injection(5mg/Kg) for seven days whereas C, C+S, and C+E groups received normal saline injection. Both C+E and D+E groups ran on a treadmill for 60 minutes/day(20minutes/4hours) at 15m/min and a 10$^{\circ}$grade for seven recovery days. Result: Post-weight(body weight before muscle dissection) of D group significantly decreased by 16.03%, and that of D+E group significantly increased by 15.51% compared with pre-weight(body weight before steroid treatment). TypeII muscle(plantaris and gastrocnemius) weights of D group were significantly lower than those of C group. Myofibrillar protein contents of typeII muscles of D group tended to decrease comparing with C group. In D+E groups, body weights and relative weights of typeII muscles(muscle weight(mg)/post-weight(g)) tended to increase comparing with D+S group. Conclusion: It is suggested that steroid- induced muscle atrophy can be ameliorated through low intensity regular exercise after dexamethasone treatment.

• Korean Journal of Biological Psychiatry
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• v.12 no.2
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• pp.136-142
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• 2005

Object:The intracellular action of the antidepressant, venlafaxine, was studied in C6-gliomas using heat shock protein 70(HSP70) immunocytochemistry and HSP70 Western blots because HSP70 is associated with stress and depression. Methods:To examine how the glucocorticoid affects the expression of HSP70 in nerve cells, the rat C6 glioma cell was treated with dexamethasone for 6 hours. In addition, venlafaxine was administered to the experimental groups of C6 glioma cells for 1, 6, 24, and 72 hours each, after which the expression of HSP70 was investigated. Finally, venlafaxine and dexamethasone were simultaneously administered to the experimental groups for 1, 6, 24, and 72 hours, followed by an investigation of the expression of HSP70. Results:The short term(1 hour) venlafaxine treatment significantly increased the level of HSP70 expression. The short term treatment of venlafaxine with dexamethasone also increased the level of HSP70 expression but this reduction was not statistically significant. The long term(72 hours) venlafaxine with dexamethasone treatment significantly reduced the level of HSP70 expression. The long term treatment of venlafaxine also reduced the level of HSP70 expression but this reduction was not statistically significant. Dexamethasone(10uM, 6hours) did not affect the level of HSP70 expression compared with controls. Conclusion:Venlafaxine increases the expression of HSP70 at short term treatment, but prolonged treatment with dexamethasone suppresses the expression of HSP70.

• Journal of Nutrition and Health
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• v.35 no.2
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• pp.207-212
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• 2002

Acetyl-CoA carboxylase (ACC) is the enzyme that controls no devo fatty acid biogynthesis, and this enzyme catalyzes the carboxylation pathway of acetyl-CoA to malonyl-CoA. Acetyl-CoA carboxylase gene expression was regulated by nutritional and hormonal status. The present study was performed to identify the regulation mechanism of ACC gene promoter I. The fragments of ACC promoter I -1.2-kb region wert recombined to pGL3-Basic vector with luciferase as a reporter gene. The primary hepatocytes from the rat were used to investigate the hormonal regulation of ACC promoter I activity. ACC PI (-1.2)/Luc plasmid was trtransferred into primary hepatocytes using lipofectin. Activity of luciferase was increased two-fold by 10-9M, three-fold by 10-8M, 10-6M, 3.5-fold by 10-6M, and 4.5-fold by 10-7M insulin treatment, respectively. In the presence of dexamethasone (1 $\mu$M), the effects of insulin increased about 1.5-fold, showing the additional effects of dexamethasone. Moreover, the activity of luciferase increased with insulin+dexamethasone, insulin+T3, dexamethasone+T3, and dexamethasone+insulin+T3 treatment approximately 6-, 4-, 6.5-, and 10-fold, respectively. Therefore it can be postulated that 1) these hormones coordinately regulate acetyl-CoA caroxylase gene expression via regulation of promoter activity, 2) the -1.2-kb region of ACC promoter I may have the response element sequences for insulin, dexamethasone, and T3.

• Korean Journal of Animal Reproduction
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• v.16 no.3
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• pp.231-237
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• 1992

The effects to the corticosteroid dexamethasone(DEX) and(or) estradiol-benzoate(E-B) treated to induction of parturition and birth weights of the young was conducted in 48 pregnant Korean native goats. The animals were divided into 4 goats per each treatment by the time(142, 145 and 148 day of pregnancy) and dosage(DEX 15, 20mg, DEX 8mg＋E-B 10mg and DEX 13mg＋E-B 7.5mg per goat). The results obtained were summarized as follows: 1 The time for induction of parturtion after DEX(15, 20mg) treatment on day 148 of pregnancy was significantly(P<0.01) shorter than 142 and 145 days. There was no significant difference each dosage of DEX on same day of pregnancy. 2. The addition of E-B to DEX treatment compared with DEX alone group at day 142 and 145 of pregnancy were significantly(P<0.01) shorter the time for induction of parturition. However, treatment with DEX along or with E-B on 148 day of pregnancy did not affect the time to induction(about 27 hrs) of parturition between each treatment. 3. The birth weight of kids after parturition was heaviest(P<0.01) on day 148 of pregnancy. However, development and vigor of kids were not significant different between DEX alone treatment and with E-B.