Immune regulation mechanism of Astragaloside IV on RAW264.7 cells through activating the NF-κB/MAPK signaling pathway.

The present study was designed to investigate the effects of Astragaloside IV (ASIV) on the immune functions of RAW264.7 cells. Compared with control group, the concentrations of interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α) and nitric oxide (NO) were higher in the 100μg/mL ASIV-treatment group. The interleukin 6 (IL-6) concentration was significantly higher in the 50 and 100μg/mL ASIV-treatment groups. The relative mRNA expression levels of IL-1β, TNF-α and inducible nitric oxide synthase (iNOS) were significantly higher in the 50 and 100μg/mL ASIV-treatment groups. The relative mRNA expression levels of IL-6 in the 100μg/mL ASIV-treatment group were significantly higher. In contrast, the relative mRNA expression levels of interleukin 4 (IL-4) and IL-6 markedly reduced in ASIV-treatment groups. Furthermore, ASIV promoted the secretion of CD40 and CD86 and increased the number of cells in G2/M phase. The apoptosis of RAW264.7 cells was decreased in ASIV-treatment groups. The protein levels of cyclin D1, CDK4 and CDK6, p50 and p-p65 increased in a dose-dependent manner. The ratio of p50/β-actin was significantly higher in the 50 and 100μg/mL ASIV-treatment groups, and p-p65/p65 was significantly higher in the 25, 50 and 100μg/mL ASIV-treatment groups. The phosphorylation levels of p38, ERK and JNK increased, and the protein expression of total p38, ERK and JNK decreased in a dose-dependent manner. These effects of ASIV were alleviated by PDTC. ASIV enhances the immune function of RAW264.7 cells by activating the NF-κB/MAPK signaling pathway.