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

Abstract

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.