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Planar catechin increases bone mass by regulating differentiation of osteoclasts in mice.

Authors :
Sugawara, Daiki
Sakai, Nobuhiro
Sato, Yurie
Azetsu, Yuki
Karakawa, Akiko
Chatani, Masahiro
Mizuno, Mirei
Maruoka, Yasubumi
Myers, Mie
Fukuhara, Kiyoshi
Takami, Masamichi
Source :
Journal of Oral Biosciences; Mar2024, Vol. 66 Issue 1, p196-204, 9p
Publication Year :
2024

Abstract

While catechins have been reported to exhibit potential to benefit osteoporosis patients, the effects of planar catechin (PCat), synthesized during the development of drugs for Alzheimer's disease, have not been clearly elucidated. Here, we examined the effects of PCat on mouse bone metabolism both in vivo and in vitro. Six week old female mice were orally administered PCat (30 mg/kg) every other day for four weeks, and their femurs were analyzed using micro-computed tomography imaging. Osteoclasts and osteoblasts were collected from mice and cultured with PCat. Subsequently, osteoclast formation and differentiation and osteoblast differentiation were observed. Mice orally administered PCat displayed significantly increased femur bone mass compared to the control group. Quantitative polymerase chain reaction findings indicated that PCat addition to osteoclast progenitor cultures suppressed osteoclast formation and decreased osteoclast marker expression without affecting the proliferative potential of the osteoclast progenitor cells. Addition of PCat to osteoblast cultures increased osteoblast marker expression. PCat inhibits osteoclast differentiation and promotes osteoblast differentiation, resulting in increased bone mass in mice. These results suggest that PCat administration is a promising treatment option for conditions associated with bone loss, including osteoporosis. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
13490079
Volume :
66
Issue :
1
Database :
Supplemental Index
Journal :
Journal of Oral Biosciences
Publication Type :
Academic Journal
Accession number :
175834619
Full Text :
https://doi.org/10.1016/j.job.2024.01.009