N-acetyl-chitooligosaccharide attenuates inflammatory responses by suppression of NF-κB signaling, MAPK and NLRP3 inflammasome in macrophages
Autor: | Hui Xia, Zou Xiaojuan, Zhigang Zhang, Haiming Hu, Daizhi Tian, Yao Xiaowei, Mingzhu Yin, Xinyu Li, Hongtao Liu |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
MAPK/ERK pathway Lipopolysaccharide Protein subunit Medicine (miscellaneous) IκB kinase Pharmacology NF-κB 03 medical and health sciences chemistry.chemical_compound 0404 agricultural biotechnology Functional saccharide medicine TX341-641 Inflammation 030109 nutrition & dietetics Nutrition and Dietetics Chemistry Nutrition. Foods and food supply Inflammasome N-acetyl-chitooligosaccharide 04 agricultural and veterinary sciences 040401 food science NLRP3 inflammasome Blockade Nf κb signaling Phosphorylation Food Science medicine.drug |
Zdroj: | Journal of Functional Foods, Vol 78, Iss, Pp 104364-(2021) |
ISSN: | 1756-4646 |
Popis: | N-acetyl-chitooligosaccharide (NACOS), prepared from the shells of shrimp and crabs, has displayed various biological activities. As prebiotics and dietary supplements, these bioactive materials can be incorporated into functional foods and beverages. This study aimed to explore the anti-inflammatory effects and associated mechanism of NACOS in macrophages. We found that NACOS reduced the levels of inflammation-related cytokines in lipopolysaccharide stimulated RAW264.7 macrophages. NACOS attenuated NF-κB activation not only through the repressed IKK phosphorylation but also the blunted nuclear translocation of NF-κB subunit p65. Additionally, NACOS inhibited the level of p-JNK. Moreover, NACOS promoted NLRP3 degradation, accompanied by the blockade of caspase-1 activation and IL-1β maturation in human THP-1 cells. This study demonstrated for the first time that NACOS has a negative effect against NLRP3 protein and NLRP3 inflammasome activation. It was suggested that the pharmacological intervention of inflammatory responses by NACOS should be a promising approach against inflammation-related clinical complications. |
Databáze: | OpenAIRE |
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