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자료유형
학술저널
저자정보
Joo, Seong-Soo (Department of Immunology, College of Pharmacy, Chung-Ang University) Won, Tae-Joon (Department of Immunology, College of Pharmacy, Chung-Ang University) Kang, Hee-Cheol (Department of Immunology, College of Pharmacy, Chung-Ang University) Lee, Do-Ik (Department of Immunology, College of Pharmacy, Chung-Ang University)
저널정보
대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제27권 제1호
발행연도
2004.1
수록면
99 - 105 (7page)

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Isoflavones have been a central subject in research on the natural phytoestrogens found in Leguminosae. Their effects on bone formation and remodeling are important in that they can act like estrogen by binding on estrogen receptors on the target cell surface. We, therefore, believed that isoflavones may help in the treatment of patients with estrogen deficiency disease such as estrogen replacement therapy (ERT) for osteoporosis. As commonly known, osteoporosis is one of the hormonal deficiency diseases, especially in menopausal women. When estrogen is no longer produced in the body a remarkable bone remodeling process occurs, and the associated events are regulated by growth factors in the osteoblast lineage. In the present study, we investigated whether isoflavones (Isocal) extracted from Sophorae fructus affect the growth factors IGF-I and TGF-$\beta$ that have been known to be related with bone formation. In the study, we found that the active control (PIII) effectively enhanced the level of nitric oxide (NO) and growth factors, and thereby inhibited osteoclastogenesis. The most efficient concentration was $10^{-8}$% within five days, whereas the comparative control (soybean isoflavone) was not as effective even at a lower concentration. In conclusion, the products which contain enriched glucosidic isoflavone and nutrient supplements such as shark cartilage and calcium can be used for osteoporosis therapy by enhancing the production of IGF-I and TGF-$\beta$. Furthermore, the NO produced through endothelial constitutive NO synthase (ecNOS) may playa role in inhibiting bone reabsorption.

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