Isoflavones extracted from Sophorae fructus upregulate IGF-I and TGF-beta and inhibit osteoclastogenesis in rat bone marrow cells.
Arch Pharm Res
; 27(1): 99-105, 2004 Jan.
Article
em En
| MEDLINE
| ID: mdl-14969347
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 play a role in inhibiting bone reabsorption.
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Base de dados:
MEDLINE
Assunto principal:
Fator de Crescimento Insulin-Like I
/
Células da Medula Óssea
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Regulação para Cima
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Fator de Crescimento Transformador beta
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Remodelação Óssea
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Genisteína
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Sophora
Idioma:
En
Ano de publicação:
2004
Tipo de documento:
Article