IL-10 Attenuates Inflammation Via MyD88/NF-κB Signal Pathway Depression

Objective To investigate the effects of IL-10 on lipopolysaccharide(LPS)-induced MyD88/NF-κB signaling activation.Methods Ana-1 macrophages were divided into a LPS group and a LPS+IL-10 group.The cells and the culture supernatant were collected at 0,0.5,1,and 2 hours respectively.The expression levels of NF-κB p65 and MyD88 in cytoplasm and nucleus were detected by Western blotting.The concentration of TNF-α in the culture supernatant was determined by ELISA.Results Through 0 to 2 hours,MyD88 expression increased significantly after LPS stimulation.The expression was attenuated by the pretreatment of IL-10,which returned to normal levels at 2 hours(8.8±0.3 vs 21.4±1.8,P0.05).IL-10 had no effect on total expression of NF-κB,but decreased nuclei/cytoplasm ratio of NF-κB p65 after LPS stimulation.The ratio was lower in the LPS+IL-10 group compared and the LPS group at 1 hour and 2 hour (1.1±0.1 vs 2.4±0.4,0.6±0.7 vs 3.1±0.6,P0.05).Consequently,IL-10 pretreatment decreased TNF-α concentration after LPS stimulation at 1 hour and 2 hours[(222.5±33.5) pg/mL vs (365.2±22.7) pg/mL,(212.7±15.9) pg/mL vs (566.2±31.5) pg/mL,P0.05].Conclusion IL-10 attenuates inflammation via MyD88/NF-κB signal pathway depression.