Abstract: Abstract: Objective To investigate the effect of interleukin (IL) -4 on MyD88/NF-κB signaling pathway in Ana-1 cells induced by lipopolysaccharides (LPS). Methods The mouse macrophages Ana-1 were divided into LPS group (given 50 μg/L LPS stimulation) and LPS+IL-4 group (given LPS stimulation after 10 μg/L IL-4 pre-culture for 1 hour). Cell culture supernatants were collected at 0, 0.5, 1 and 2 hours. The relative expression levels of MyD88 and NF-κB mRNA were detected by RT-PCR. The expression levels of MyD88, total protein of NF - κB and NF - κB p65 were detected by Western blot assay. The content ratio in nucleus and cytoplasm of NF-κB p65 and the contents of interleukin (IL)-6 and tumor necrosis factor (TNF)-α in cell culture supernatant were detected by ELISA. Results With the prolongation of cell culture time, the expression levels of MyD88 and NF-κB mRNA and proteins, the ratio of NF-κB p65 nuclei/cytoplasm, IL- 6 and TNF-a levels increased gradually (P＜0.05). There was no significant difference in the expression of MyD88 in LPS+ IL-4 group (P＞0.05). The expression of MyD88 protein, NF-κB mRNA and protein, the nuclear/cytoplasmic ratio of NF- κB p65 and levels of IL-6 and TNF-α increased first and then decreased (P＜0.05). The expression of MyD88 protein, the nuclear/cytoplasmic ratio of NF-κB p65 and levels of IL-6 and TNF-α at 1 h and 2 h were significantly decreased in LPS+ IL-4 group than those of LPS group (P＜0.05). There were no significant differences in the expression levels of NF- κB mRNA and proteins in different time points between two groups (P＞0.05). Conclusion IL-4 may play an antiinflammatory role by inhibiting the activation of MyD88/NF-κB signaling pathway. IL-4 can down-regulate the expression of pro-inflammatory cytokines IL-6 and TNF-α.

Key words: interleukin-4, interleukin-6, lipopolysaccharides, tumor necrosis factor-alpha, myeloid differentiation factor 88, NF-kappa B, inflammation