Effects of [beta]-glucan on the release of nitric oxide by macrophages stimulated with lipopolysaccharide

• Published in: Asian-australasian journal of animal sciences Vol. 29; no. 11; p. 1664
• Main Authors: Choi, E.Y, Lee, S.S, Hyeon, J.Y, Choe, S.H, Keum, B.R, Lim, J.M, Park, D.C, Choi, I.S, Cho, K.K
• Format: Journal Article
• Language: English
• Published: Asian - Australasian Association of Animal Production Societies 01.11.2016
• Subjects: Glucans; Health aspects; Lipopolysaccharides; Macrophages; Nitric oxide
• ISSN: 1011-2367
• DOI: 10.5713/ajas.16.0418

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. (Key Words: [beta]-Glucan, Lipopolysaccharide [LPS], Nitric Oxide [NO], RAW 264.7 Cells, STAT1)