The inhibition of LPS-induced inflammation in RAW264.7 macrophages via the PI3K/Akt pathway by highly N-acetylated chitooligosaccharide.

Chitooligosaccharide (COS) has been shown to regulate many biological functions, such as antimicrobial effect and antitumor activity. In the present study, highly N-acetylated chitooligosaccharide (NACOS) was prepared by N-acetylation of COS, and the anti-inflammatory activity of NACOS in macrophages were evaluated. The results indicated NACOS significantly suppressed the LPS-induced pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) expression. Furthermore, the increased levels of reactive oxygen species (ROS) and nitric oxide (NO) were repressed by NACOS in a dose dependent manner. However, NACOS itself had no significant effect on the cell viability and cellular morphology. Signal transduction studies demonstrated that NACOS remarkably inhibited LPS-enhanced phosphorylation of phosphatidylinositol 3-kinase (PI3K) and Akt. These findings provide a possible molecular mechanism by which NACOS inhibit LPS-induced inflammatory response in macrophages, and a basis for utilizing NACOS in pharmaceutical therapy against inflammation.