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Kmeria duperreana (Pierre) Dandy Extract Suppresses LPS-Induced iNOS and NO via Regulation of NF-κB Pathways and p38 in Murin Macrophage RAW 264.7 Cells
Development of anti-inflammatory products remains in high demand due to the incidence of inflammatory diseases, including diabetes, cardiovascular disease, and neurodegenerative diseases. In this study, we examined the potential anti-inflammatory activity of the nutraceutical, Kmeria duperreana (Pie...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Society of Food Science and Nutrition
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7333012/ https://www.ncbi.nlm.nih.gov/pubmed/32676468 http://dx.doi.org/10.3746/pnf.2020.25.2.166 |
Sumario: | Development of anti-inflammatory products remains in high demand due to the incidence of inflammatory diseases, including diabetes, cardiovascular disease, and neurodegenerative diseases. In this study, we examined the potential anti-inflammatory activity of the nutraceutical, Kmeria duperreana (Pierre) Dandy extract (KDE). We evaluated the ability of KDE to inhibit lipopolysaccharide (LPS)-induced inflammatory markers, including nitric oxide (NO), nuclear factor kappa-B, and mitogen-activated protein kinases, in RAW 264.7 cells. KDE suppressed LPS-induced nitrite production and inducible NO synthase (iNOS) expression in RAW 264.7 cells, but has no effect on cyclooxygenase-2 expression. KDE also suppressed LPS-induced phosphorylation of p65, IκB kinase, and p38 in RAW 264.7 cells. Through Western blot assays and immunofluorescence results, we showed that KDE suppresses LPS-induced p65 translocation from cytosol to the nucleus in RAW 264.7 cells. Moreover, KDE suppressed mRNA expression of LPS-induced interleukin (IL)-1β in RAW 264.7 cells, but had no effect on mRNA expression of IL-6 or tumor necrosis factor-a. These results demonstrate that KDE may be a promising anti-inflammatory nutraceutical. KDE may act by suppressing iNOS expression and subsequent NO production by inhibiting phosphorylation of p65 and p38 and suppressing translocation of p65 from the cytosol to the nucleus. |
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