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Naringenin inhibits human osteoclastogenesis and osteoclastic bone resorption.

Abstract：

BACKGROUND AND OBJECTIVE:Naringenin, a naturally occurring flavonoid, possesses a wide range of pharmacological properties. The purpose of this study was to investigate the effect of naringenin on human osteoclastogenesis and osteoclastic bone resorption. MATERIAL AND METHODS:Naringenin was tested in a human osteoclastogenesis model using primary osteoclast precursor cells activated by receptor activator of nuclear factor-kappaB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) for 6 days. Osteoclastogenesis was assessed by determining the number of tartrate-resistant acid phosphatase (TRAP)-stained multinuclear cells, while the secretion of factors involved in osteoclastogenesis was assessed using enzyme-linked immunosorbent assays. The effect of naringenin on bone resorption was investigated using an OsteoAssay human bone plate coupled with an immunoassay to evaluate the release of helical peptide 620-633 from the alpha1 chain of type I collagen. RESULTS:Naringenin was non-toxic at the highest concentration used (50 microg/ml). Naringenin (10, 25 and 50 microg/ml) significantly inhibited osteoclastogenesis (by 29 +/- 5, 57 +/- 8 and 96 +/- 1%, respectively). Naringenin also markedly inhibited the secretion of interleukin (IL)-1alpha (by 59%), IL-23 (by 87%) and monocyte chemoattractant protein-1 (by 58%). Lastly, naringenin (10, 25 and 50 microg/ml) significantly decreased the release of helical peptide 620-633, an indicator of bone resorption activity (by 44 +/- 0.5, 73 +/- 0.5 and 86 +/- 1%, respectively). CONCLUSIONS:Naringenin can inhibit human osteoclastogenesis and osteoclastic bone resorption. It thus holds promise as a therapeutic or preventive agent for bone-related diseases such as periodontitis.

journal_name

J Periodontal Res

journal_title

Journal of periodontal research

authors

La VD,Tanabe S,Grenier D

doi

10.1111/j.1600-0765.2008.01107.x

subject

Has Abstract

pub_date

2009-04-01 00:00:00

pages

193-8

issue

2

eissn

0022-3484

issn

1600-0765

pii

JRE1107

journal_volume

44

pub_type

杂志文章

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