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8 results on '"G. S. Jeong"'

4. Placenta Hominis Protects Osteoporosis in Ovariectomized Rats

Author

Soo-Wan Chae, Han-Jung Chae, Geun-Youn Lee, S. K. Yoo, G. S. Jeong, H. R. Park, Su-Jin Kim, H I Choi, K H Choi, Hye-Lin Kim, Taekyun Shin, and Hyung-Ryong Kim

Subjects
endocrine system, medicine.medical_specialty, Bone density, Ovariectomy, Placenta, Immunology, Osteoporosis, Osteoclasts, Cell Count, Toxicology, Bone and Bones, Rats, Sprague-Dawley, Bone Density, Pregnancy, Trabecular Meshwork, Osteoclast, Internal medicine, Animals, Humans, Immunology and Allergy, Medicine, Osteoporosis, Postmenopausal, Pharmacology, Osteoblasts, Femur Neck, Tissue Extracts, business.industry, Body Weight, Osteoblast, General Medicine, medicine.disease, Biomechanical Phenomena, Rats, Trabecular bone, surgical procedures, operative, medicine.anatomical_structure, Endocrinology, Disease Progression, Ovariectomized rat, Alkaline phosphatase, Female, business, Biomarkers, hormones, hormone substitutes, and hormone antagonists
Abstract

In China, Japan, and Korea, placenta hominis extracts (PHEs) are used clinically for the treatment of osteoporosis. The anti-osteoporotic effect of PHEs was studied. The trabecular bone area and thickness in OVX rats decreased by 50% from those in sham-operated rats; these decreases were completely inhibited by administration of PHEs for 7 weeks. Osteoclast numbers and the osteoblast surface were enhanced in OVX rats, but PHEs had no effect on these phenomena. Serum phosphorus and alkaline phosphatase in OVX rats increased compared to those in sham-operated rats, but the increases were not affected by the administration of PHEs. Thyroxine (T4) level was stimulated in OVX rats. The extracts inhibited the T4 level in the OVX rats. These results strongly suggest that PHEs be effective in preventing the development of bone loss induced by OVX in rats.

Published
2006
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5. Yuk-Hap-Tang Induces Apoptosis by Intervening Mn-SOD in Human Cervical Carcinoma HeLa Cells

Author

Han-Jung Chae, J. M. Park, Geun-Youn Lee, G. S. Jeong, Soo-Wan Chae, Hye-Lin Kim, H. R. Park, Se-Gun Kim, S. K. Yoo, and Hyung-Ryong Kim

Subjects
Programmed cell death, Cell Survival, Poly ADP ribose polymerase, Apoptosis, Antioxidants, HeLa, chemistry.chemical_compound, Humans, Cytotoxicity, Caspase, Medicine, East Asian Traditional, Korea, biology, Plant Extracts, Superoxide Dismutase, Free Radical Scavengers, General Medicine, Glutathione, biology.organism_classification, Molecular biology, Kinetics, Complementary and alternative medicine, chemistry, Caspases, Cancer cell, biology.protein, HeLa Cells, Phytotherapy
Abstract

Yuk-Hap-Tang (YHT) induces cell death in human cervical carcinoma HeLa cells. Caspase-3, -6 and -9 were markedly activated in HeLa cells treated with YHT. The preferred substrate for caspase-3 cysteine protease, PARP, was cleaved to its 85-kDa cleavage product. YHT increased the amount of the anti-apoptotic protein, Bcl-2, and the pro-apoptotic protein, Bax. Although p53 has been reported to accumulate in cancer cells in response to anticancer agents, the p53 expression level was not changed in HeLa cells treated with YHT. Manganese (Mn)-TBAP, a mitochondria-specific SOD mimetic agent and NAC/GSH (N-acetyl cysteine/reduced glutathione) reduced the YHT-induced cytotoxicity and decreased the number of the YHT-induced apoptotic cells. Furthermore, YHT reduced the expression of Mn-SOD protein and its activity in HeLa cells. The data demonstrate that YHT induces the apoptosis of human cervical carcinoma HeLa cells by intervening Mn-SOD.

Published
2004
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8. Costunolide inhibits production of tumor necrosis factor-α and interleukin-6 by inducing heme oxygenase-1 in RAW264.7 macrophages.

Author

G.-S. Jeong, H.-S. Kim, W. Woo, H. Rhew, H. Kim, D. Sohn, and Y.-C. Kim

Subjects
*TUMOR necrosis factors, *INTERLEUKIN-6, *HEME oxygenase, *MACROPHAGES
Abstract

Abstract. Objectives:  Heme oxygenase (HO)-1 expression via nuclear factor-erythroid 2-related factor 2 (Nrf2) activation has an ability to inhibit tumor necrosis factor (TNF)-α and interleukin (IL)-6 production. Costunolide has been reported to inhibit IL-1 production, but whether other cytokines could be inhibited remains to be confirmed. We investigated the effects of costunolide and its components (α-methylene-γ-butyrolactone; CH2-BL, α-methyl-γ-butyrolactone; CH3-BL, and γ-butyrolactone; BL) on HO-1 expression as well as TNF-α and IL-6 production in RAW264.7 macrophages. Methods:  HO-1 expression and Nrf2 nuclear accumulation were analyzed by Western blot analysis. The production of TNF-α and IL-6 in RAW264.7 macrophages stimulated with lipopolysaccharide (LPS) was assayed by ELISA. Results:  Costunolide and CH2-BL induced HO-1 expression and Nrf2 nuclear accumulation, whereas CH3-BL and BL did not. Pre-incubation with costunolide inhibited LPS-induced production of TNF-α and IL-6. The inhibitory effects of costunolide on TNF-α and IL-6 production were abrogated by tin protoporphyrin, an HO inhibitor. Conclusions:  Costunolide is an effective HO-1 inducer capable of inhibiting macrophage-derived pro-inflammatory cytokines. CH2-BL moiety of costunolide is essential for Nrf2 activation leading to HO-1 expression. [ABSTRACT FROM AUTHOR]

Published
2007

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