Abstract
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-κB pathway in human THP-1 macrophages induced by lipopolysaccharide (LPS). The results showed that the concentrations of TNF-α and IL-1β released from LPS stimulated THP-1 cells increased significantly compared to control (p < 0.01). After treatment with APS, the TNF-α and IL-1β levels were significantly lower than those in the LPS group (p < 0.05). The mRNA expression of TNF-α and IL-1β were also inhibited. Mechanistic studies indicated that APS strongly suppressed NF-κB activation and down-regulated the phosphorylation of ERK and JNK, which are important signaling pathways involved in the production of TNF-α and IL-1β, demonstrating that APS could suppress the production of TNF-α and IL-1β by LPS stimulated macrophages by inhibiting NF-κB activation and ERK and JNK phosphorylation.
Highlights
Inflammation plays an important role in the progression of many diseases, including cardiovascular diseases, cancer and autoimmune diseases, such as rheumatoid arthritis (RA) [1,2,3,4,5]
Different concentrations of Astragalus polysaccharides (APS) could lower the level of TNF- and IL-1β, and there was a significant difference compared with the LPS group (p < 0.05, p < 0.01)
To determine whether MAPK signaling pathways are involved in the anti-inflammatory effects of APS, we investigated the phosphorylation of two MAPK signaling molecules, ERK1/2 and JNK, by Western blot
Summary
Inflammation plays an important role in the progression of many diseases, including cardiovascular diseases, cancer and autoimmune diseases, such as rheumatoid arthritis (RA) [1,2,3,4,5]. Many researchers have demonstrated that macrophages, the key inflammatory cells, are closely associated with the pathologic process of inflammation [6,7]. They have three major functions in inflammatory response: antigen presentation, phagocytosis, and immunomodulation through production of various cytokines and growth factors, such as TNF- and IL-1β [8]. It was able to reduce cell accumulation, swelling and arthritic index of the joints and serum concentrations of inflammatory mediators in adjuvant arthritic (AA) rats
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