Preventive effects of a Kampo Medicine, Kakkonto, on inflammatory responses via the suppression of extracellular Signal-Regulated Kinase Phosphorylation in Lipopolysaccharide-Treated human gingival fibroblasts Article ID 784019

• Material Type: 博士論文
• ISSN: 2090-5165
• Title: Preventive effects of a Kampo Medicine, Kakkonto, on inflammatory responses via the suppression of extracellular Signal-Regulated Kinase Phosphorylation in Lipopolysaccharide-Treated human gingival fibroblasts
• Volume: 2014 Article ID 784019
• Author/Editor: Kitamura, Hiroyuki; Urano, Hiroko; Ara, Toshiaki; 喜多村, 洋幸
• Publication Date: 2014-02-18
• Publication Date (W3CDTF): 2014-02-18
• Alternative Title: LPS 刺激ヒト歯肉線維芽細胞におけるExtracellular Signal-Regulated Kinase のリン酸化抑制を介した葛根湯の炎症反応抑制効果
• Periodical title: ISRN pharmacology
• Degree grantor/type: 松本歯科大学
• Date Granted: 2015-02-05
• Date Granted (W3CDTF): 2015-02-05
• Dissertation Number: 甲第160号
• Degree Type: 博士（歯学）
• Conferring No. (Dissertation): 甲第160号
• Text Language Code: eng
• Subject Heading: Anti-Inflammatory Agents; Medicine Kampo; Gingiva cytology; gingiva drug effects; Lipopolysaccharide; Kakkonto
• Note (General): Periodontal disease is accompanied by inflammation of the gingiva and destruction of periodontal tissues, leading to alveolar bone loss in severe clinical cases. The chemical mediator prostaglandin E2 (PGE2) and cytokines such as interleukin- (IL-)6 and IL-8 have been known to play important roles in inflammatory responses and tissue degradation. In the present study, we investigated the effects of a kampo medicine, kakkonto (TJ-1), on the production of prostaglandin E2 (PGE2), IL-6, and IL-8 by human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS) from Porphyromonas gingivalis. Kakkonto concentration dependently suppressed LPS-induced PGE2 production but did not alter basal PGE2 levels. In contrast, kakkonto significantly increased LPSinduced IL-6 and IL-8 production. Kakkonto decreased cyclooxygenase- (COX-)1 activity to approximately 70% at 1mg/mL but did not affect COX-2 activity. Kakkonto did not affect cytoplasmic phospholipase A2 (cPLA2), annexin1, or LPS-induced COX-2 expression. Kakkonto suppressed LPS-induced extracellular signal-regulated kinase (ERK) phosphorylation, which is known to lead to ERK activation and cPLA2 phosphorylation. These results suggest that kakkonto decreased PGE2 production by inhibition of ERK phosphorylation which leads to inhibition of cPLA2 phosphorylation and its activation. Therefore, kakkonto may be useful to improve gingival inflammation in periodontal disease.; 2014; identifier:甲第160号; PubMed番号 : 24693448; 元資料の権利情報 : Copyright © 2014 Hiroyuki Kitamura et al. This is an open access article distributed under the Creative Commons Attribution License(https://creativecommons.org/licenses/by/3.0/); 元資料の権利情報 : CC BY
• DOI: info:doi/10.1155/2014/784019; https://doi.org/info:doi/10.1155/2014/784019
• Persistent ID (NDL): info:ndljp/pid/9491164; https://dl.ndl.go.jp/pid/9491164
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2015-09-01T13:12:47+09:00
• Date Created (W3CDTF): 2015-07-06
• Format (IMT): PDF
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Original Material (URI): 雑誌掲載論文(電子版); http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945151/
• Periodical Title (URI): http://id.nii.ac.jp/1070/00002396/
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp