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  • 标题:Comparison of Inhibitory Effects of Polyanions on Nitric Oxide Production by Macrophages Stimulated with LPS
  • 本地全文:下载
  • 作者:Masaki Otsuka ; Seishi Tsuchiya ; Yukihiko Aramaki
  • 期刊名称:Biological and Pharmaceutical Bulletin
  • 印刷版ISSN:0918-6158
  • 电子版ISSN:1347-5215
  • 出版年度:2006
  • 卷号:29
  • 期号:3
  • 页码:499-502
  • DOI:10.1248/bpb.29.499
  • 出版社:The Pharmaceutical Society of Japan
  • 摘要:In this paper, we investigated the inhibitory mechanism of the production of nitric oxide (NO) by polyanions and liposomes composed of phosphatidylserine (PS-liposomes) focusing on cytokine production and mitogen activated protein kinase (MAP kinase) activation. NO production by macrophages was inhibited by treatment with oxidized lipoprotein (OxLDL), maleylated bovine serum albumin (mBSA), and heparin. No inhibitory effect was exhibited by poly-cytidilic acid (PolyC). To clarify the mechanism of the inhibitory effect of polyanions on NO production, we evaluated the productions of transforming growth factor-β (TGF-β) and interleukin (IL)-10 which are known to be anti-inflammatory cytokines. TGF-β was produced when macrophages were treated with OxLDL as was the case with PS-liposomes. No increase in TGF-β production was observed for mBSA, heparin, and PolyC. On the other hand, significant production of IL-10 was observed using mBSA. Extracellular signal-regulated kinase (ERK), a member of the MAP kinase superfamily, was activated when macrophages were treated with OxLDL as well as PS-liposomes. In the case of mBSA, the activation of ERK and c-Jun N-terminal kinase (JNK) was observed. No activation of p38 MAP kinase was observed using any of the polyanions. Although heparin had an inhibitory effect on NO production by macrophages, no activation of MAP kinase or production of TGF-β and IL-10 was observed. The inhibitory effect of these ligands on NO production may be regulated via different signaling pathways.
  • 关键词:nitric oxide (NO);macrophage;polyanion;mitogen activated protein (MAP) kinase;transforming growth factor-β (TGF-β);interleukin (IL)-10
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