Effects of β-Glucan on the Release of Nitric Oxide by Macrophages Stimulated with Lipopolysaccharide
العنوان: | Effects of β-Glucan on the Release of Nitric Oxide by Macrophages Stimulated with Lipopolysaccharide |
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المؤلفون: | S. H. Choe, J. M. Lim, Kwang-Keun Cho, Sung-Lim Lee, D. C. Park, In Soon Choi, B. R. Keum, Eun Young Choi, J. Y. Hyeon |
المصدر: | Asian-Australasian Journal of Animal Sciences, Vol 29, Iss 11, Pp 1664-1674 (2016) ASIAN-AUSTRALASIAN JOURNAL OF ANIMAL SCIENCES(29): 11 Asian-Australasian Journal of Animal Sciences |
بيانات النشر: | Asian-Australasian Association of Animal Production Societies, 2016. |
سنة النشر: | 2016 |
مصطلحات موضوعية: | 0301 basic medicine, Lipopolysaccharide, p38 mitogen-activated protein kinases, lcsh:Animal biochemistry, medicine.disease_cause, beta-Glucan, Lipopolysaccharide [LPS], Nitric Oxide [NO], RAW 264.7Cells, STAT1, Article, Microbiology, Nitric oxide, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, β-Glucan, medicine, Escherichia coli, lcsh:QP501-801, lcsh:SF1-1100, biology, Activator (genetics), Chemistry, Kinase, Molecular biology, 030104 developmental biology, RAW 264.7 Cells, 030220 oncology & carcinogenesis, biology.protein, Phosphorylation, Animal Science and Zoology, lcsh:Animal culture, Food Science |
الوصف: | 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. |
اللغة: | English |
تدمد: | 1976-5517 1011-2367 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fdf50c6fa39ec6209ba1853f98fcd92e http://www.ajas.info/upload/pdf/ajas-29-11-1664.pdf |
حقوق: | OPEN |
رقم الأكسشن: | edsair.doi.dedup.....fdf50c6fa39ec6209ba1853f98fcd92e |
قاعدة البيانات: | OpenAIRE |
تدمد: | 19765517 10112367 |
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