• Proceedings of the Korean Nutrition Society Conference
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• 1997.11b
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• pp.31-31
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• 1997

• Proceedings of the Ginseng society Conference
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• 1997.05a
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• pp.14-14
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• 1997

• Tuberculosis and Respiratory Diseases
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• v.54 no.1
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• pp.15-21
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• 2003

Background : There are many risk factors for osteoporosis in patients with chronic obstructive pulmonary disease(COPD). These include smoking, a low body mass index, insufficient exercise, and the use of glucocortcoids. However, there is lack of data on the incidence of osteoporosis according to the different glucocorticoid administration methods in patients with COPD. This study compared the incidence of osteoporosis according to the different administration methods of glucocorticoid. Methods : A matched case-controlled study (gender, age, cumulative steroid dose and pack-years of smoking) was conducted. Forty-five patients with documented COPD for at least a 3 year duration and a cumulative glucocorticoid dose above 1,000 mg were enrolled in study. The patients were classified into the following three groups. First, fifteen patients received continuous inhaled glucocorticoid with intermittent oral steroids but had no admission history due to an acute exacerbation(Group I). Secondly, fifteen patients received a multiple course of oral steroids with additional inhaled glucocorticoid but had no admission history due to their acute exacerbation(Group II). Lastly, fifteen patients received intermittent oral or inhaled glucocorticoids and had an admission history due to the acute exacerbation with intravenous steroid treatment for at least 2 weeks per year(Group III). The enrolled patients had apulmonary function test and bone densitometry performed at the lumbar spine and femoral neck. Results : The patients from Group III had significantly high incidence of osteoporosis in the lumbar and femoral neck compared to Group I and Group II (p<0.01). Conclusion : The incidence of osteoporosis in patients with COPD appears to be strongly affected by the method of steroid administration. This result suggests that intravenous steroid administration is strongly associated with the risk of osteoporosis.

• BMB Reports
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• v.43 no.8
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• pp.524-529
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• 2010

Glucocorticoids (GCs) are useful drugs for the treatment of various diseases, but their use for prolonged periods can cause severe side effects such as osteoporosis. GCs have a direct effect on bone cells, where they can arrest bone formation, in part through the inhibition of osteoblast. On the other hand, GCs potently suppress osteoclast resorptive activity by disrupting its cytoskeleton based on the inhibition of RhoA, Rac and Vav3 in response to macrophage colony-stimulating factor. GCs also interfere with microtubule distribution and stability, which are critical for cytoskeletal organization in osteoclasts. Thus, GCs inhibit microtubule-dependent cytoskeletal organization in osteoclasts, which, in the context of bone remodeling, further dampens bone formation.

• Journal of Society of Preventive Korean Medicine
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• v.10 no.2
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• pp.19-30
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• 2006

It is well known that glucocorticoid may induce osteoporosis as its side effect in long-term therapy. The inhibition of osteoblast by glucocorticoid is also recognized as its action mechanism of decreased bone formation. In this study, the effect of DSG, Danchisoyosangamibang, on the differentiation and function of osteoblastic cells was investigated. The osteoblastic cells were isolated from rat calvariae using collagenase treatment. The cell counting, enzyme activity assay, MTT assay, collagen content assay were done to determine the cell proliferation, intracellular alkaline phosphatase (ALP) activity, bone martrix production, and cell apoptosis. DSG enhanced the cell proliferation after the culture for 10 days. ALP activity and total protein synthesis, and intracelluar collagen synthesis were increased time dependently when the cells were treated with DSG in the presence of dexamethasone. And, DSG restored calvarial cell function decreased by dexamethasone.

• The Journal of Natural Sciences
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• v.9 no.1
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• pp.25-29
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• 1997

To study the mechanism of lipocortin-1, the 37 kDa protein, one of the annxin superfamily thought to be a second messenger during the Glucocorticoid dependent anti-inflammatory action, the gene for lipocortin-1 binding protein was isolated using the yeast two hybrid assay, the yeast based genetic assay recognizing the protein-protein interaction. The results showed that this gene has a weak homology to the for the human serine proteinase.

• Archives of Pharmacal Research
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• v.10 no.3
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• pp.184-187
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• 1987

ln order to develope anti-inflammatory glucocorticoids for local use without systemic side-effects, ester and amide derivatives of 20$\xi$-dihydroprednisolonic acid have been prepared. When binding affinities of these compounds to glucocorticoid receptor of rat liver cytosol were compared, all a-isomer at C-20 showed higher binding affinities than the corres¬ponding $\beta$-isomer. The size of the substituents at C-21 had significant influences on binding affinities, which were related with their lipophilicity.

• Proceedings of the Ginseng society Conference
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• 2008.05a
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• pp.76-76
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• 2008

• Journal of Society of Preventive Korean Medicine
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• v.12 no.2
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• pp.197-206
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• 2008

The inhibition of osteoblast by glucocorticoid is recognized as its action mechanism of decreased bone formation. In this study, the effect of JY, Jahyulyangkeuntang, on the differentiation and mineralization of osteoblastic cells was investigated in the presence of dexamethasone. The cell counting, enzyme activity assay, MTT assay, collagen content assay were done to determine the cell proliferation, alkaline phosphatase(ALP) activity, bone martrix production, and cell apoptosis. JY enhanced the cell proliferation after the culture for 10 days. ALP activity and total protein synthesis, and intracellular collagen synthesis were increased when the cells were treated with JY. And JY restored calvarial cell function decreased by dexamethasone.

• The Korean Journal of Pharmacology
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• v.3 no.1
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• pp.27-29
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• 1967

Many investigators reported the mineral corticoid hormon-like action of Glycyrrhizin. The other investigators suggested concerning the glucocorticoid hormon-like action. Authors had been observed the glycogen content of the liver to make sure the relationship between glucocorticoid like action of Glycyrrhizin and glucose metabolism in the liver. There was significant increase in the liver glycogen content in rat fed Glycyrrhizin for two weeks, however it was confirmed that Glucuronic acid combined with Glucuronic was unable to make any influence to glycogen content. The relation concerning the effect of Glycyrrhizin on liver glycogen and its mechanism of action might be needed followup study.