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Chrysin Derivative CM1 and Exhibited Anti-Inflammatory Action by Upregulating Toll-Interacting Protein Expression in Lipopolysaccharide-Stimulated RAW264.7 Macrophage Cells.
Byun, Eui-Baek; Song, Ha-Yeon; Kim, Woo Sik; Han, Jeong Moo; Seo, Ho Seong; Park, Woo Yong; Kim, Kwangwook; Byun, Eui-Hong.
Afiliación
  • Byun EB; Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, Jeongeup 56212, Korea.
  • Song HY; Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, Jeongeup 56212, Korea.
  • Kim WS; Functional Biomaterial Research Center, Korea Research Institute of Bioscience and Biotechnology, Jeongeup 56212, Korea.
  • Han JM; Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, Jeongeup 56212, Korea.
  • Seo HS; Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute, Jeongeup 56212, Korea.
  • Park WY; Department of Pharmacology, College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea.
  • Kim K; Department of Food Science and Technology, Kongju National University, Yesan 32439, Korea.
  • Byun EH; Department of Food Science and Technology, Kongju National University, Yesan 32439, Korea.
Molecules ; 26(6)2021 Mar 11.
Article en En | MEDLINE | ID: mdl-33799689
Although our previous study revealed that gamma-irradiated chrysin enhanced anti-inflammatory activity compared to intact chrysin, it remains unclear whether the chrysin derivative, CM1, produced by gamma irradiation, negatively regulates toll-like receptor (TLR) signaling. In this study, we investigated the molecular basis for the downregulation of TLR4 signal transduction by CM1 in macrophages. We initially determined the appropriate concentration of CM1 and found no cellular toxicity below 2 µg/mL. Upon stimulation with lipopolysaccharide (LPS), CM1 modulated LPS-stimulated inflammatory action by suppressing the release of proinflammatory mediators (cytokines TNF-α and IL-6) and nitric oxide (NO) and downregulated the mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) signaling pathways. Furthermore, CM1 markedly elevated the expression of the TLR negative regulator toll-interacting protein (Tollip) in dose- and time-dependent manners. LPS-induced expression of cell surface molecules (CD80, CD86, and MHC class I/II), proinflammatory cytokines (TNF-α and IL-6), COX-2, and iNOS-mediated NO were inhibited by CM1; these effects were prevented by the knockdown of Tollip expression. Additionally, CM1 did not affect the downregulation of LPS-induced expression of MAPKs and NF-κB signaling in Tollip-downregulated cells. These findings provide insight into effective therapeutic intervention of inflammatory disease by increasing the understanding of the negative regulation of TLR signaling induced by CM1.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Flavonoides / Péptidos y Proteínas de Señalización Intracelular / Macrófagos Límite: Animals Idioma: En Revista: Molecules Asunto de la revista: BIOLOGIA Año: 2021 Tipo del documento: Article Pais de publicación: Suiza
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Flavonoides / Péptidos y Proteínas de Señalización Intracelular / Macrófagos Límite: Animals Idioma: En Revista: Molecules Asunto de la revista: BIOLOGIA Año: 2021 Tipo del documento: Article Pais de publicación: Suiza