Immunoregulatory polysaccharides from Apocynum venetum *** stimulate phagocytosis and cytokine expression via activating the NF-κB/MAPK signaling pathways in RAW264.7 cells
Immunoregulatory polysaccharides from Apocynum venetum *** stimulate phagocytosis and cytokine expression via activating the NF-κB/MAPK signaling pathways in RAW264.7 cells作者机构:National R&D Center for Edible Fungus Processing TechnologyHenan UniversityKaifeng 475004China Functional Food Engineering Technology Research CenterKaifeng 475004China School of Chemical SciencesUniversity of AucklandAuckland 1142New Zealand Joint International Research Laboratory of Food&Medicine Resource FunctionKaifeng 475004China
出 版 物:《Food Science and Human Wellness》 (食品科学与人类健康(英文))
年 卷 期:2022年第11卷第4期
页 面:806-814页
核心收录:
学科分类:1008[医学-中药学(可授医学、理学学位)] 0832[工学-食品科学与工程(可授工学、农学学位)] 1006[医学-中西医结合] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 100602[医学-中西医结合临床] 10[医学]
基 金:supported by Research on Precision Nutrition and Health Food Department of Science and Technology of Henan Province(CXJD2021006)
主 题:Apocynum venetum L.flowers Immunomodulatory polysaccharide RAW264.7 cells NF-κB signaling pathway MAPK signaling pathway
摘 要:Two immunomodulatory polysaccharides(Vp2a-Ⅱ and Vp3) were isolated and identified from Apocynum venetum L. flowers, and their innate immune-stimulating functions and working mechanisms were evaluated in RAW264.7 cells. Both the level of released nitric oxide(NO) and expression of inducible nitric oxide synthase(iNOS) m RNA were significantly enhanced in the RAW264.7 macrophages cells treated by Vp2a-Ⅱ and Vp3. Vp2a-Ⅱ(100–800 μg/m L) and Vp3(400 μg/mL) could significantly increase the phagocytic activity of RAW264.7 cells and the secretion and m RNA expression of TNF-α and IL-6 in a concentrationdependent manner through affecting mitogen-activated protein kinase(MAPK) activity and nuclear factor κB(NF-κB) nuclear translocation. Vp2a-Ⅱ might activate the MAPK signaling pathways and induce the nuclear translocation of NF-κB p65, whilst Vp3 likely activated the NF-κB and MAPK signaling pathways without influencing the p38 MAPK route.