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  • 标题:Curcumin suppresses the production of interleukin-6 in Prevotella intermedia lipopolysaccharide-activated RAW 264.7 cells
  • 本地全文:下载
  • 作者:Kim, Sung-Jo
  • 期刊名称:The Journal of the Korean Academy of Periodontology
  • 印刷版ISSN:0250-3352
  • 出版年度:2011
  • 卷号:41
  • 期号:3
  • 页码:157-163
  • DOI:10.5051/jpis.2011.41.3.157
  • 语种:English
  • 出版社:Korean Academy of Periodontology
  • 摘要:Purpose

    Curcumin is known to exert numerous biological effects including anti-inflammatory activity. In this study, we investigated the effects of curcumin on the production of interleukin-6 (IL-6) by murine macrophage-like RAW 264.7 cells stimulated with lipopolysaccharide (LPS) from Prevotella intermedia , a major cause of inflammatory periodontal disease, and sought to determine the underlying mechanisms of action.

    Methods

    LPS was prepared from lyophilized P. intermedia ATCC 25611 cells by the standard hot phenol-water method. Culture supernatants were collected and assayed for IL-6. We used real-time polymerase chain reaction to detect IL-6 mRNA expression. IκB-α degradation, nuclear translocation of NF-κB subunits, and STAT1 phosphorylation were characterized via immunoblotting. DNA-binding of NF-κB was also analyzed.

    Results

    Curcumin strongly suppressed the production of IL-6 at both gene transcription and translation levels in P. intermedia LPS-activated RAW 264.7 cells. Curcumin did not inhibit the degradation of IκB-α induced by P. intermedia LPS. Curcumin blocked NF-κB signaling through the inhibition of nuclear translocation of NF-κB p50 subunit. Curcumin also attenuated DNA binding activity of p50 and p65 subunits and suppressed STAT1 phosphorylation.

    Conclusions

    Although further study is required to explore the detailed mechanism of action, curcumin may contribute to blockade of the host-destructive processes mediated by IL-6 and appears to have potential therapeutic values in the treatment of inflammatory periodontal disease.

  • 关键词:Curcumin; Periodontal disease; Prevotella intermedia; Lipopolysaccharides; Interleukin-6
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