• 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.

• Journal of Veterinary Clinics
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• v.26 no.6
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• pp.534-538
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• 2009

Antiemetic effect of dexamethasone in dogs sedated with medetomidine was evaluated. On the day of experiment, five minutes prior to medetomidine ($40\;{\mu}g$/kg, IM) injection, dexamethasone was administered intravenously at the doses of 0.25, 0.5 and 1.0 mg/kg. Control group was received at 0.1 ml/kg of saline instead of dexamethasone. The dose of 0.5 and 1.0 mg/kg of dexamethasone significantly reduced emetic episode. The degree of sedation determined by visual sedation scoring was not influenced by dexamethasone pretreatments. In addition, the values of complete blood counts and blood chemistry did not show significant changes and were within normal ranges before and the day after experiment. These results show that the doses of 0.5 and 1.0 mg/kg of dexamethasone are useful and safe method to prevent emetic episode inducing by medetomidine in dogs, without evidence of any clinically relevant influences.

• 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.

• Tuberculosis and Respiratory Diseases
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• v.84 no.3
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• pp.217-225
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• 2021

Background: Despite the proven benefits of dexamethasone in hospitalized coronavirus disease 2019 (COVID-19) patients, the optimum time for the administration of dexamethasone is unknown. We investigated the progression of COVID-19 pneumonia based on the timing of dexamethasone administration. Methods: A single-center, retrospective cohort study based on medical record reviews was conducted between June 10 and September 21, 2020. We compared the risk of severe COVID-19, defined as the use of a high-flow nasal cannula or a mechanical ventilator, between groups that received dexamethasone either within 24 hours of hypoxemia (early dexamethasone group) or 24 hours after hypoxemia (late dexamethasone group). Hypoxemia was defined as room-air SpO₂ <90%. Results: Among 59 patients treated with dexamethasone for COVID-19 pneumonia, 30 were in the early dexamethasone group and 29 were in the late dexamethasone group. There was no significant difference in baseline characteristics, the time interval from symptom onset to diagnosis or hospitalization, or the use of antiviral or antibacterial agents between the two groups. The early dexamethasone group showed a significantly lower rate of severe COVID-19 compared to the control group (75.9% vs. 40.0%, p=0.012). Further, the early dexamethasone group showed a significantly shorter total duration of oxygen supplementation (10.45 days vs. 21.61 days, p=0.003) and length of stay in the hospital (19.76 days vs. 27.21 days, p=0.013). However, extracorporeal membrane oxygenation and in-hospital mortality rates were not significantly different between the two groups. Conclusion: Early administration of dexamethasone may prevent the progression of COVID-19 to a severe disease, without increased mortality.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.2
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• pp.127-135
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• 1999

As part of a study on the effects of dexamethasone and dehydroepiandrosterone (DHEA) on the biological roles of astrocytes in brain injury, this study evaluated the effects of dexamethasone and DHEA on the responses of primary cultured rat cortical astrocytes to lipopolysaccharide (LPS) and antimycin A. Dexamethasone decreased spontaneous release of LDH from astrocytes, and the dexamethasone effect was inhibited by DHEA. However, the inhibitory effect of DHEA on the dexamethasone-induced decrease of LDH release was not shown in astrocytes treated with LPS, and antimycin A-induced LDH release was not affected by dexamethasone or DHEA. Unlike dexamethasone, DHEA increased MTT value of astrocytes and also attenuated the antimycin A-induced decrease of MTT value. Glutamine synthetase activity of astrocytes was not affected by DHEA or LPS but increased by dexamethasone, and the dexamethasone- dependent increase was attenuated by DHEA. However, antimycin A markedly decreased glutamine synthetase activity, and the antimycin A effect was not affected by dexamethasone or DHEA. Basal release of $[^3H]arachidonic$ acid from astrocytes was moderately increased by LPS and markedly by antimycin A. Dexamethasone inhibited the basal and LPS-dependent releases of $[^3H]arachidonic$ acid, but neither dexamethasone nor DHEA affected antimycin A-induced $[^3H]arachidonic$ acid release. Basal IL-6 release from astrocytes was not affected by dexamethasone or DHEA but markedly increased by LPS and antimycin A. LPS-induced IL-6 release was attenuated by dexamethasone but was little affected by DHEA, and antimycin A-induced IL-6 release was attenuated by DHEA as well as dexamethasone. At the concentration of dexamethasone and DHEA which does not affect basal NO release from astrocytes, they moderately inhibited LPS-induced NO release but little affected antimycin A-induced decrease of NO release. Taken together, these results suggest that dexamethasone and DHEA, in somewhat different manners, modulate the astrocyte reactivity in brain injuries inhibitorily.

• Korean Journal of Ichthyology
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• v.19 no.2
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• pp.88-92
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• 2007

The effect of dexamethasone injection on the burden of marine birnavirus (MABV) in asymptomatically infected olive flounder (Paralichthys olivaceus) fingerlings was investigated. In real time PCR analysis, the threshold cycle (Ct) value of the fish injected with dexamethasone was significantly lower than that of the fish in the PBS-injected and no-handling groups. The higher amplification of the MABV gene in the dexamethasone-injected group than the 2 control groups was confirmed also by semi-quantitative RT-PCR. The results indicate an increase of MABV burden in olive flounder fingerlings after a single injection with dexamethasone.

• YAKHAK HOEJI
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• v.53 no.2
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• pp.78-82
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• 2009

We explored the effects of dexamethasone on osteoclast precursors using BMMs. Dexamethasone inhibited the proliferation of BMMs. Furthermore, it stimulated the osteoclast formation via NFATc1 activation in the presence of RANKL. Since dexamethasone targeted the early stage of osteoclast formation, we investigated its effect on mRNA expression of GR and $IFN-{\beta}$. Whereas dexamethasone had no effects on GR expression in the presence of RANKL, it reduced the expression of $IFN-{\beta}$, suggesting that dexamethasone increased RANKL-induced osteoclast formation by modulating $IFN-{\beta}$.

• 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.

• 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 Pain
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• v.21 no.1
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• pp.51-56
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• 2008

Background: Preoperative dexamethasone improves the surgical outcome after laparoscopic cholecystectomy(LC). The purpose of this study was to determine the effect of preoperative dexamethasone on the postoperativepain according to age and gender in patients who undergo LC.Methods: In this double blind prospective study, 400 patients, males or females :< 45 yr and males or femaless 65 yr (n = 50 in each of eight groups) who undergoing LC were randomized to receive dexamethasone 8mg (5 ml) or saline 5 ml intravenously 100 minutes before their operation, Postoperative pain was assessedon a visual analog scale (VAS) at 1, 6, 12, and 24 hour, and the time to administering the first postoperativeanalgesics was recorded.Results: Dexamethasone was administered without consideration for age and gender, and it reduced thepostoperative pain VAS score at 1, 6, and 12 hours, and the opioid analgesic requirement, but there was nosignificant difference between administering saline or dexamethasone in the same gender and age groups.Females U 45 yr who were administered saline had the most pain sensitivity and males S 65 yr who wereadministered dexamethasone had the least pain sensitivity.Conclusions: Preoperative dexamethasone reduces the pain intensity and opioid consumption, but does notreduce the pain intensity, according to age and gender in the patients undergoing LC. As a result, Preoperativedexamethasone should be considered for routine use for patients who are undergoing laparoscopic cho-lecystectomy. (Korean J Pain 2008; 21: 51 56)