Abstract
This research analyzed the effect of β-glucan that is expected to alleviate the production of the inflammatory mediator in a macrophagocyte, which was processed by the lipopolysaccharide (LPS) of Escherichia, a pathogen related to allergy. The incubated layer was used for a nitric oxide (NO) analysis. The DNA-binding activation of the small unit of NF-κB was measured using the ELISA-based kit. In the RAW264.7 cells that were vitalized by E.coli LPS, the β-glucan inhibited both the combatant and rendering phases of the inducible NO synthase (iNOS)-derived NO. β-glucan increased the expression of the heme oxygenase-1 (HO-1) in the cell that was stimulated by E.coli LPS, and the HO-1 activation was inhibited by the SnPP. This shows that the NO production induced by LPS is related to the inhibition effect of β-glucan. The phosphorylation of JNK and the p38 induced by the LPS were not influenced by the β-glucan, and the IκB-α decomposition was not influenced either. Instead, β-glucan remarkably inhibited the phosphorylation of the STAT1 that was induced by the E.coli LPS. Overall, the β-glucan inhibited the production of NO in the macrophagocyte that was vitalized by the E.coli LPS through the HO-1 induction and the STAT1 pathways inhibition in this research. As the host inflammation reaction control by β-glucan weakens the progress of the allergies, β-glucan can be used as an effective treatment method.
Note: This abstract was not presented at the conference.
Citation Format: Kwang Keun Cho, Sr. The study of β-glucan on the release of nitric oxide by macrophages stimulated with lipopolysaccharide. [abstract]. In: Proceedings of the AACR Special Conference: Improving Cancer Risk Prediction for Prevention and Early Detection; Nov 16-19, 2016; Orlando, FL. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2017;26(5 Suppl):Abstract nr B21.
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