論文

査読有り
2015年3月

Catechins inhibit vascular endothelial growth factor production and cyclooxygenase-2 expression in human dental pulp cells

INTERNATIONAL ENDODONTIC JOURNAL
  • T. Nakanishi
  • ,
  • K. Mukai
  • ,
  • Y. Hosokawa
  • ,
  • D. Takegawa
  • ,
  • T. Matsuo

48
3
開始ページ
277
終了ページ
282
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1111/iej.12312
出版者・発行元
WILEY-BLACKWELL

AimTo investigate the effect of catechins on vascular endothelial growth factor (VEGF) production and cyclooxygenase-2 (COX-2) expression in human dental pulp cells (HDPC) stimulated with bacteria-derived factors or pro-inflammatory cytokines.
MethodologyMorphologically fibroblastic cells established from explant cultures of healthy human dental pulp tissues were used as HDPC. HDPC pre-treated with catechins, epigallocatechin-3-gallate (EGCG) or epicatechin gallate (ECG), were exposed to lipopolysaccharide (LPS), peptidoglycan (PG), interlukin-1 (IL-1) or tumour necrosis factor- (TNF-). VEGF production was examined by enzyme-linked immunosorbent assay, and COX-2 expression was assessed by immunoblot.
ResultsEGCG and ECG significantly reduced LPS- or PG-mediated VEGF production in the HDPC in a dose-dependent manner. EGCG also prevented IL-1-mediated VEGF production. Although TNF- did not enhance VEGF production in the dental pulp cells, treatment of 20gmL(-1) of EGCG decreased the level of VEGF. In addition, the catechins attenuated COX-2 expression induced by LPS and IL-1.
ConclusionsThe up-regulated VEGF and COX-2 expressions in the HDPC stimulated with these bacteria-derived factors or IL-1 were diminished by the treatment of EGCG and ECG. These findings suggest that the catechins may be beneficial as an anti-inflammatory tool of the treatment for pulpal inflammation.

Web of Science ® 被引用回数 : 8

リンク情報
DOI
https://doi.org/10.1111/iej.12312
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/24847951
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000349621600010&DestApp=WOS_CPL