Inhibitory Effect of Astragalus Polysaccharides on Lipopolysaccharide-Induced TNF-α and IL-1β Production in THP-1 Cells

被引:101
作者
He, Xiaojuan [1 ]
Shu, Jun [2 ]
Xu, Li [3 ]
Lu, Cheng [1 ]
Lu, Aiping [1 ,4 ]
机构
[1] China Acad Chinese Med Sci, Inst Basic Res Clin Med, Beijing 100700, Peoples R China
[2] China Japan Friendship Hosp, Inst Clin Med Sci, Beijing 100029, Peoples R China
[3] Beijing Univ Chem Technol, Coll Life Sci & Technol, Beijing 100029, Peoples R China
[4] Hong Kong Baptist Univ, Sch Chinese Med, Kowloon, Hong Kong, Peoples R China
基金
美国国家科学基金会;
关键词
Astragalus polysaccharides; anti-inflammatory; macrophage; MAPK; NF-kappa B; NF-KAPPA-B; RHEUMATOID-ARTHRITIS; RECEPTOR ACTIVATOR; SIGNALING PATHWAY; KINASE; MACROPHAGES; THERAPY; TAK1; INFLAMMATION; DISEASE;
D O I
10.3390/molecules17033155
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Astragalus polysaccharides (APS), one of main bioactive components in Astragalus membranaceus Bunge, has been reported to possess anti- inflammatory activities, but the molecular mechanisms behind this activity are largely unknown. This study aimed to investigate expression of inflammatory cytokines and the MAPK/NF-kappa B pathway in human THP-1 macrophages induced by lipopolysaccharide (LPS). The results showed that the concentrations of TNF-alpha and IL-1 beta released from LPS stimulated THP-1 cells increased significantly compared to control (p < 0.01). After treatment with APS, the TNF-alpha and IL-1 beta levels were significantly lower than those in the LPS group (p < 0.05). The mRNA expression of TNF-alpha and IL-1 beta were also inhibited. Mechanistic studies indicated that APS strongly suppressed NF-kappa B activation and down-regulated the phosphorylation of ERK and JNK, which are important signaling pathways involved in the production of TNF-alpha and IL-1 beta, demonstrating that APS could suppress the production of TNF-alpha and IL-1 beta by LPS stimulated macrophages by inhibiting NF-kappa B activation and ERK and JNK phosphorylation.
引用
收藏
页码:3155 / 3164
页数:10
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