2026-03-06T14:31:40Z https://mdu.repo.nii.ac.jp/oai

oai:mdu.repo.nii.ac.jp:00002408 2023-06-19T07:56:49Z 170:218

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 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 喜多村, 洋幸 Kitamura, Hiroyuki Urano, Hiroko Ara, Toshiaki Anti-Inflammatory Agents Medicine Kampo Gingiva cytology gingiva drug effects Lipopolysaccharide Kakkonto 松本歯科大学 博士（歯学） 2014 甲第160号 application/pdf 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. doctoral thesis 2014-02-18 2015-02-05 VoR ISRN pharmacology Article ID 784019 2014 甲第160号 2090-5165 https://mdu.repo.nii.ac.jp/records/2408 eng 雑誌掲載論文(電子版) PubMed Central® (PMC) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945151/ info:pmid/24693448 info:doi/10.1155/2014/784019 https://doi.org/10.1155/2014/784019 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/) open access