Effects of β-Glucan on the Release of Nitric Oxide by Macrophages Stimulated with Lipopolysaccharide

  • Choi, E.Y. (Department of Life Science, Silla University) ;
  • Lee, S.S. (Division of Applied Life Science, Graduate School of Gyeongsang National University, IALS) ;
  • Hyeon, J.Y. (Department of Life Science, Silla University) ;
  • Choe, S.H. (Department of Life Science, Silla University) ;
  • Keum, B.R. (Department of Life Science, Silla University) ;
  • Lim, J.M. (Glucan Corporation) ;
  • Park, D.C. (Glucan Corporation) ;
  • Choi, I.S. (Department of Life Science, Silla University) ;
  • Cho, K.K. (Department of Animal Resources Technology, Gyeongnam National University of Science and Technology)
  • Received : 2016.05.26
  • Accepted : 2016.07.19
  • Published : 2016.11.01


This research analyzed the effect of ${\beta}$-glucan that is expected to alleviate the production of the inflammatory mediator in macrophagocytes, which are processed by the lipopolysaccharide (LPS) of Escherichia. The incubated layer was used for a nitric oxide (NO) analysis. The DNA-binding activation of the small unit of nuclear factor-${\kappa}B$ was measured using the enzyme-linked immunosorbent assay-based kit. In the RAW264.7 cells that were vitalized by Escherichia coli (E. coli) LPS, the ${\beta}$-glucan inhibited both the combatant and rendering phases of the inducible NO synthase (iNOS)-derived NO. ${\beta}$-Glucan increased the expression of the heme oxygenase-1 (HO-1) in the cells that were stimulated by E. coli LPS, and the HO-1 activation was inhibited by the tin protoporphyrin IX (SnPP). This shows that the NO production induced by LPS is related to the inhibition effect of ${\beta}$-glucan. The phosphorylation of c-Jun N-terminal kinases (JNK) and the p38 induced by the LPS were not influenced by the ${\beta}$-glucan, and the inhibitory ${\kappa}B-{\alpha}$ ($I{\kappa}B-{\alpha}$) decomposition was not influenced either. Instead, ${\beta}$-glucan remarkably inhibited the phosphorylation of the signal transducer and activator of transcription-1 (STAT1) that was induced by the E. coli LPS. Overall, the ${\beta}$-glucan inhibited the production of NO in macrophagocytes that was vitalized by the E. coli LPS through the HO-1 induction and the STAT1 pathways inhibition in this research. As the host immune response control by ${\beta}$-glucan weakens the progress of the inflammatory disease, ${\beta}$-glucan can be used as an effective immunomodulator.


${\beta}$-Glucan;Lipopolysaccharide [LPS];Nitric Oxide [NO];RAW 264.7 Cells;STAT1


Supported by : Ministry of Trade, Industry, and Energy, Korea


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