• Journal of Korean Medicine Rehabilitation
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• v.20 no.1
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• pp.37-59
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• 2010

Objectives : The object of this study was to observe the favorable anti arthritic effects of Euiiin-tang($y{\grave{i}}y{\breve{i}}r{\acute{e}}n-t{\bar{a}}ng$) aqueous extract(EIITe), has been traditionally used in Korean medicine for treating rheumatoid arthritis on collagen induced arthritic(CIA) DBA/1 mice. Methods : In the present study, effects of EIITe on the releases of human tumor necrosis factor(TNF)-${\alpha}$, interleukin(IL)-$1{\beta}$, matrix metalloproteinase(MMP)-13 and production of Nitric oxide(NO) were observed by in vitro. In addition, to observe the effects on the CIA mice, three different dosages of EIITe, 300, 150 and 150 mg/kg were orally administered once a day for 18 days from 24hrs after antigen challenges(type II collagen) on 21 days after immunization using Type II collagen Freund's complete adjuvant. Six groups, each of 8 DBA/1 mice per group were used in the present study as follows. Changes on the body weights, macroscopic arthritis scores, splenic weights, splenic TNF-${\alpha}$ and IL-6 contents, articular cartilage(femur and tibia) collagen and glycosaminoglycans-chondroitin sulphate, sulphate and hyaluronic acid contents, histopathological observations(microscopic arthritis scores, thicknesses of femur and tibia cartilage thicknesses were monitored, compared to that of dexamethasone, a potent anti inflammatory agents, 1 mg/kg treated mice. Results : As results of collagen challenges, marked decreases of body weights and gains, articular cartilage collagen and glycosaminoglycan - chondroitin sulphate, sulphate and hyaluronic acid contents were observed with increases of macroscopic arthritis scores, splenic weights, splenic TNF-${\alpha}$ and IL-6 contents, articular cartilage(in the both femur and tibia) loss and damages. However, these CIA signs were significantly and dosages dependently inhibited by treatment of EIITe 300 and 150 mg/kg as compared with CIA control, respectively. In addition, the releases of TNF-${\alpha}$, IL-$1{\beta}$, NO and MMP-13 were markedly and dose dependently inhibited by treatment of EIITe, invitro. Although CIA were more favorably inhibited by treatment of dexamethasone 1 mg/kg as compared with EIITe 300 mg/kg, marked decreases of body weights were detected in dexamethasone 1 mg/kg treated mice. Conclusions : The results obtained in this study suggest that over 150 mg/kg of EIITe showed favorable anti arthritic effects on the CIA mediated by immunomodulatory and/or anti oxidative effects. However, detail mechanism studies should be conduced in future with the screening of the biological active compounds in this herb. lthough CIA were more favorably inhibited by treatment of dexamethasone 1 mg/kg as compared with EIITe 300 mg/kg, marked decreases of body weights were detected in dexamethasone 1 mg/kg treated mice, in the present study.

• Clinical and Experimental Pediatrics
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• v.46 no.10
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• pp.989-995
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• 2003

Purpose : Dexamethasone is frequently administered to prevent or treat chronic lung disease in human neonates who are also prone to hypoxic-ischemic(HI) insults. Recently, meta-analysis of the follow-up studies reveals a significantly increased odd ratio for the occurrence of cerebral palsy or an abnormal neurologic outcome, and there is conflicting evidence regarding the impact of dexamethasone exposure on HI brain injury. This study was conducted to explore the effect of post-HI dexamethasone administration on neuronal injury in neonatal rats. Methods : HI was produced in seven-day-old rats by right carotid artery ligation followed by two hours of 8% oxygen exposure. At the end of HI, the animals were injected intraperitoneally either with dexamethasone(0.5 mg/kg) or saline. Neuronal injury was assessed seven days after the HI by the area of infarction, TUNEL reactivity, Bcl-2 and Bax expression in brain. Results : Post-insult dexamethasone administration resulted in reduction of weight gain and a higher mortality rate during seven days after HI. Dexamethasone treatment revealed no effect on the size of brain infarction induced by HI. Bax protein expression increased in dexamethasone treated brain but Bcl-2 protein expression and TUNEL reactivity revealed no significant differences between dexamethasone treated and non treated brain. Increased Bax protein expression suggest upregulation of the apoptosis by dexamethasone. Conclusion : The result suggests the adverse role of Post-HI administration of dexamethasone in neonatal HI.

• Journal of Veterinary Science
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• v.22 no.3
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• pp.33.1-33.6
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• 2021

Very virulent infectious bursal disease virus (vvIBDV) causes high mortality in chickens but measures to reduce the mortality have not been explored. Chickens (8-9 weeks) were treated with 3 agents before and during vvIBDV inoculation. Dexamethasone treatment reduced the mortality of infected chickens (40.7% vs. 3.7%; p < 0.001), but treatment with aspirin or vitamin E plus selenium did not affect the mortality. The bursa of Fabricius appeared to have shrunk in both dead and surviving chickens (p < 0.01). The results indicate that dexamethasone can reduce mortality in vvIBDV-infected chickens and may provide therapeutic clues for saving individual birds infected by the virus.

• IMMUNE NETWORK
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• v.14 no.6
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• pp.328-332
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• 2014

Dexamethasone (Dex) was shown to inhibit the differentiation, maturation, and antigen-presenting function of dendritic cells (DC) when added during DC generation or maturation stages. Here, we examined the direct effects of Dex on MHC-restricted antigen processing. Macrophages were incubated with microencapsulated ovalbumin (OVA) in the presence of different concentrations of Dex for 2 h, and the efficacy of OVA peptide presentation was evaluated using OVA-specific CD8 and CD4 T cells. Dex inhibited both class I- and class II-restricted presentation of OVA to T cells; this inhibitory effect on antigen presentation was much more potent in immature macrophages than in mature macrophages. The presentation of the exogenously added OVA peptide SIINFEKL was not blocked by Dex. In addition, short-term treatment of macrophages with Dex had no discernible effects on the phagocytic activity, total expression levels of MHC molecules or co-stimulatory molecules. These results demonstrate that Dex inhibits intracellular processing events of phagocytosed antigens in macrophages.

• Clinical and Experimental Pediatrics
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• v.57 no.3
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• pp.101-109
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• 2014

The use of glucocorticoids (GCs) in the perinatal period is suspected of being associated with adverse effects on long-term neurodevelopmental outcomes for preterm infants. Repeated administration of antenatal GCs to mothers at risk of preterm birth may adversely affect fetal growth and head circumference. Fetal exposure to excess GCs during critical periods of brain development may profoundly modify the limbic system (primarily the hippocampus), resulting in long-term effects on cognition, behavior, memory, co-ordination of the autonomic nervous system, and regulation of the endocrine system later in adult life. Postnatal GC treatment for chronic lung disease in premature infants, particularly involving the use of dexamethasone, has been shown to induce neurodevelopmental impairment and increases the risk of cerebral palsy. In contrast to studies involving postnatal dexamethasone, long-term follow-up studies for hydrocortisone therapy have not revealed adverse effects on neurodevelopmental outcomes. In experimental studies on animals, GCs has been shown to impair neurogenesis, and induce neuronal apoptosis in the immature brains of newborn animals. A recent study has demonstrated that dexamethasone-induced hypomyelination may result from the apoptotic degeneration of oligodendrocyte progenitors in the immature brain. Thus, based on clinical and experimental studies, there is enough evidence to advice caution regarding the use of GCs in the perinatal period; and moreover, the potential long-term effects of GCs on brain development need to be determined.

• Korean Journal of Veterinary Service
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• v.41 no.1
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• pp.47-49
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• 2018

A 2-month-old female Holstein Friesian calf was noted to leak urine from the umbilicus during urination. She urinated through both the umbilicus and the urethra. A conduit from the umbilicus to the bladder was identified with ultrasonography. Uroperitoneum was ruled out because blood urea nitrogen and creatinine were within reference ranges. Surgery was performed to resect the patent urachus. Urachitis was identified during surgery. Dexamethasone and an antibiotic were used for the inflammation and postoperative cares. Meloxicam was substituted for dexamethasone since the calf showed side effects to dexamethasone. The calf recovered completely and there was no urine leakage from the umbilicus.

• Osong Public Health and Research Perspectives
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• v.9 no.6
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• pp.334-339
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• 2018

Objectives: Human rhinoviruses (HRVs) are the major cause of the common cold. Currently there is no registered, clinically effective, antiviral chemotherapeutic agent to treat diseases caused by HRVs. In this study, the antiviral activity of dexamethasone (DEX) against HRV1B was examined. Methods: The anti-HRV1B activity of DEX was assessed by sulforhodamine B assay in HeLa cells, and by RT-PCR in the lungs of HRV1B-infected mice. Histological evaluation of HRV1B-infected lungs was performed and a histological score was given. Anti-HRV1B activity of DEX via the glucocorticoid receptor (GCR)-dependent autophagy activation was assessed by blocking with chloroquine diphosphate salt or bafilomycin A1 treatment. Results: In HRV1B-infected HeLa cells, treatment with DEX in a dose-dependent manner, resulted in a cell viability of > 70% indicating that HRV1B viral replication was reduced by DEX treatment. HRV1B infected mice treated with DEX, had evidence of reduced inflammation and a moderate histological score. DEX treatment showed antiviral activity against HRV1B via GCR-dependent autophagy activation. Conclusion: This study demonstrated that DEX treatment showed anti-HRV1B activity via GCR-dependent autophagy activation in HeLa cells and HRV1B infected mice. Further investigation assessing the development of topical formulations may enable the development of improved DEX effectiveness.

• Design & Manufacturing
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• v.17 no.1
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• pp.40-47
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• 2023

Macular degeneration and glaucoma are representative age-related retinal diseases that rank second and third in the prevalence of retinal diseases, and are a kind of degenerative neurological disease. Irreversible visual acuity and visual field damage may occur, and the number of patients is rapidly increasing as the population ages. Since this retinal disease is a chronic disease, continuous drug treatment is required. There are various drug delivery methods for treatment, but direct injection of the drug into the intravitreal is the most effective for continuous delivery of the drug over a long period of time. In order to solidify Dexamethasone, a retinal disease treatment, and insert it into the primary intravitreal, it is important to develop a technology to miniaturize the treatment and an applicator to deliver the treatment. In this study, a mold technology was developed to integrate the cannula and hub, which are one part of applicator. In addition, surface treatment was performed on the outside of the cannula to improve the bonding strength between the cannula and the hub, and the bonding strength according to each condition was analyzed through a tensile test.

• Journal of Korean Medicine Rehabilitation
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• v.23 no.2
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• pp.49-61
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• 2013

Objectives : This study was conducted to determine whether or not Kangwhaldoche-tang(Qianghuodaozhi-tang) (KDT) aqueous extracts can protect articular cartilage losses on the Freund's complete adjuvant(FCA)-induced rat rheumatoid arthritis. Methods : 520, 260 or 130 mg/kg of KDT were orally administered once a day for 14 days from 14 days after FCA treatments, and 15 mg/kg of dexamethasone was intraperitoneally administered as reference drug in this experiment. Changes on the body weight, knee circumferences, gross arthritis score, inflammatory tissue prostaglandin(PG) $E_2$ levels were monitored with cartilage collagen components and glucosaminoglycans(GAGs) compositions - chondroitin sulphate, heparin sulphate and hyaluronic acid in the present study. Results : As results of FCA treatment, classic rheumatoid arthritis featuring dramatic decreases of the body weights, cartilage collagen and GAGs contents with increases of the knee circumferences, gross arthritis scores and inflammatory tissue $PGE_2$ levels, were demonstrated in the present study. However, these changes from FCA - induced rheumatoid arthritis were clearly inhibited by treatment of dexamethasone and all three different dosages of KDT. Although overall anti-inflammatory effects of KDT 520 mg/kg were lowered than those of dexamethasone 15 mg/kg treated rats, KDT 520 mg/kg showed more favorable preserve effects on the cartilage GAGs and KDT 260 mg/kg treated rats showed similar preserve effects as compared with dexamethasone 15 mg/kg in this experiment. Conclusions : The present results supported that over 75 mg/kg of KDT showed favorable anti-arthritic effects on the FCA-induced arthritis mediated by suppression of $PGE_2$, representative inflammatory mediator, and may help improve rheumatoid arthritis.

• Toxicological Research
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• v.3 no.2
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• pp.73-80
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• 1987

Primary cultures of adult rat hepatocytes were used to study the cytotoxicity of D-galactosamine. Hepatocytes were isolated by a collagenase perfusion technique and maintained as monolayers in serum-free medium on collagen-coated culture dishes. Treatment of galactosamine to the culture markedly inhibited the uptake of ${\alpha}$-aminoisobutyric acid (AIB) inducible with glucagon and dexamethasone. At0.1 mM of galactosamine, AIB uptake was inhibited significantly when treated for 12 hr. At higher doses (0.25, 0.5 and 1.0mM), a significant inhibition was noticed after 1 hr exposure. Generally the magnitude of the inhibition was related to the dose and treatment time of galactosamine. Treatment of galactosamine also produced a dose- and treatment time-related suppression of the tyrosine aminotransferase (TAT) induction caused by dexamethasone. Meanwhile, uptake of ouabain was not affected by the treatment of galactosamine. The viability of the hepatocytes was decreased only slightly by the treatment of galactosamine; more than 87% of the cells excluded tryphane blue when treated 1 mM galactosamine for 12 hr. Galactosamine induced depressions of AIB uptake and TAT activity were prevented by the simultaneous addition of uridine to the culture. D-Galactosamine, cytotoxicity, hepatocytes culture, ${\alpha}$-aminoisobutyric acid uptake, tyrosine aminotransferase.