| Item type |
文献 / Documents(1) |
| 公開日 |
2018-11-12 |
| アクセス権 |
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アクセス権 |
open access |
| 資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
| 出版社版DOI |
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関連識別子 |
https://doi.org/10.1371/journal.pone.0154107 |
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関連名称 |
10.1371/journal.pone.0154107 |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| タイトル |
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|
タイトル |
Rebamipide Attenuates Mandibular Condylar Degeneration in a Murine Model of TMJ-OA by Mediating a Chondroprotective Effect and by Downregulating RANKL-Mediated Osteoclastogenesis |
| タイトル別表記 |
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その他のタイトル |
Role of Rebamipide in Mandibular Condylar Remodeling |
| 著者 |
井澤, 俊
森, 浩喜
篠原, 丈裕
三野, 彰子
Hutami, Islamy Rahma
岩浅, 亮彦
田中, 栄二
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| 抄録 |
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内容記述 |
Temporomandibular joint osteoarthritis (TMJ-OA) is characterized by progressive degradation of cartilage and changes in subchondral bone. It is also one of the most serious subgroups of temporomandibular disorders. Rebamipide is a gastroprotective agent that is currently used for the treatment of gastritis and gastric ulcers. It scavenges reactive oxygen radicals and has exhibited anti-inflammatory potential. The aim of this study was to investigate the impact of rebamipide both in vivo and in vitro on the development of cartilage degeneration and osteoclast activity in an experimental murine model of TMJ-OA, and to explore its mode of action. Oral administration of rebamipide (0.6 mg/kg and 6 mg/kg) was initiated 24 h after TMJ-OA was induced, and was maintained daily for four weeks. Rebamipide treatment was found to attenuate cartilage degeneration, to reduce the number of apoptotic cells, and to decrease the expression levels of matrix metalloproteinase-13 (MMP-13) and inducible nitric oxide synthase (iNOS) in TMJ-OA cartilage in a dose-dependent manner. Rebamipide also suppressed the activation of transcription factors (e.g., NF-κB, NFATc1) and mitogen-activated protein kinases (MAPK) by receptor activator of nuclear factor kappa-B ligand (RANKL) to inhibit the differentiation of osteoclastic precursors, and disrupted the formation of actin rings in mature osteoclasts. Together, these results demonstrate the inhibitory effects of rebamipide on cartilage degradation in experimentally induced TMJ-OA. Furthermore, suppression of oxidative damage, restoration of extracellular matrix homeostasis of articular chondrocytes, and reduced subchondral bone loss as a result of blocked osteoclast activation suggest that rebamipide is a potential therapeutic strategy for TMJ-OA. |
| 書誌情報 |
en : PLOS ONE
巻 11,
号 4,
p. e0154107,
発行日 2016-04-28
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| 収録物ID |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
19326203 |
| 出版者 |
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出版者 |
PLOS |
| 備考 |
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|
値 |
The third author's name is spelled incorrectly. The correct name is : Takehiro Shinohara. |
| 権利情報 |
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権利情報 |
Copyright: © 2016 Izawa et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
| EID |
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|
識別子 |
310860 |
| 言語 |
|
|
言語 |
eng |
pone_11_4_e0154107.pdf (1.71 MB)
