天然产物研究与开发 ›› 2014, Vol. 26 ›› Issue (1): 131-135.

• 开发研究 • 上一篇    下一篇

聚合度7-15的壳寡糖抑制脂多糖刺激的单核细胞产生TNF-α和IL-8的作用研究

李昱1,2,王文霞1,许青松1,李曙光1,杜昱光1*   

  1. 1 中国科学院大连化学物理研究所,大连116023;2 中国科学院研究生院,北京 100049
  • 出版日期:2014-01-31 发布日期:2014-12-15

Research on the Blockade Role of Chitosan Oligosaccharides with 7-15 Polymerization Degree on Expressions of TNF-α and IL-8 in Monocytes Stimulated by LPS

LI Yu1,2, WANG Wen-xia1, XU Qing-song1, LI Shu-guang1, DU Yu-guang1*   

  1. 1 Dalian Institute of chemical physics,Chinese Academy of Sciences,Dalian 116023,China;2 Graduate School of Chinese Academy of Sciences,Beijing 100049,China
  • Online:2014-01-31 Published:2014-12-15

摘要: 本文通过建立脂多糖刺激的单核细胞炎症损伤模型,观察聚合度7-15的壳寡糖对炎性单核细胞白细胞介素-8(IL-8)和肿瘤坏死因子-α(TNF-α)表达的影响,及对p38丝裂原激活的蛋白激酶(p38 mitogen-activated protein kinases,p38MAPK)信号通路磷酸化的影响。采用p38信号通路抑制剂(SB203580)验证抑制p38信号通路对脂多糖诱导的单核细胞表达IL-8和TNF-α的作用,从而探索壳寡糖抑制单核细胞炎性损伤的分子机制。结果表明壳寡糖可抑制脂多糖诱导的单核细胞表达IL-8和TNF-α,并且抑制p38信号蛋白的磷酸化水平。因此,初步认为壳寡糖可能通过抑制炎性U937细胞中p38MAPK信号通路抑制IL-8和TNF-α的表达。

关键词: 壳寡糖, 脂多糖, p38MAPK信号通路, 白细胞介素-8, 肿瘤坏死因子-&alpha

Abstract: To investigate the molecular mechanism of anti-inflammatory functions of chitosan oligosaccharides (COS),the inflammatory models of highly expressed IL-8 and TNF-α were established by LPS-stimulation.The levels of IL-8 and TNF-α in LPS-induced monocytes and the phosphorylation of p38 MAPK in inflammatory monocytes were observed.Blockage effects of p38 on deducing inflammatory response of LPSstimulated monocytes were verified by SB203580 treatment.Results showed that COS suppressed the expression of IL-8 and TNF-α and blocked the phosphorylation of p38 MAPK signaling protein in U937 cells induced by LPS.Hence,it was considered that COS might exert anti-inflammatory effects by inhibiting the production of IL-8 and TNF-α and p38 MAPK signaling pathway in LPS-stimulated U937 cells.

Key words: chitosan oligosaccharides, lipopolysaccharide, p38MAPK signaling pathway, IL-8, TNF-&alpha,

中图分类号: 

R965