RRC ID 12455
Author Choi EM.
Title Apigenin increases osteoblastic differentiation and inhibits tumor necrosis factor-alpha-induced production of interleukin-6 and nitric oxide in osteoblastic MC3T3-E1 cells.
Journal Pharmazie
Abstract Many plant-derived substances have estrogenic activities. Due to their ability to bind the estrogen receptor, these compounds have the potential to counteract the deleterious effects of estrogen deficiency on bone. In this study, the effects of apigenin on the function of osteoblastic MC3T3-E1 cells and the production of local factors in osteoblasts were investigated. Apigenin (0.01 microM) significantly increased the growth of MC3T3-E1 cells and caused a significant elevation of alkaline phosphatase (ALP) activity and collagen content in the cells (P < 0.05). The effect of apigenin in increasing ALP activity and collagen content was completely prevented by the presence of 10(-6) M cycloheximide and 10-6 M tamoxifen, suggesting that apigenin's effect results from a newly synthesized protein component and might be partly involved in estrogen action. Locally derived mediators in bone play a crucial role in the regulation of bone remodeling, i.e., bone formation and bone resorption processes. The effect of apigenin on the TNF-alpha-induced production of IL-6 and nitric oxide (NO) in osteoblasts was examined. Treatment with apigenin (10 microM) decreased the TNF-alpha-induced production of IL-6 and NO in osteoblasts. Taken together, these results suggest that apigenin may represent new pharmacological tools for the treatment of osteoporosis.
Volume 62(3)
Pages 216-20
Published 2007-3
PMID 17416199
MeSH 3T3 Cells Alkaline Phosphatase / metabolism Animals Apigenin / pharmacology* Cell Differentiation / drug effects Cell Survival / drug effects Collagen / metabolism Immunoassay Indicators and Reagents Interleukin-6 / biosynthesis* Mice Nitric Oxide / biosynthesis* Osteoblasts / drug effects* Tumor Necrosis Factor-alpha / antagonists & inhibitors*
IF 1.016
Times Cited 9
Human and Animal Cells