Abstract：The present paper aims to establish a RAW264.7 macrophage model to investigate the effects of CD36 and extracellular regulated kinase (ERK) signaling pathway on the secretion of inflammation-related cytokines induced by lipopolysaccharide (LPS). Firstly, the macrophages with or without CD36 knockdown were stimulated with 100 ng/ml LPS for 16 h. Then the activation of ERK and secretion of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) and IL-10 were analyzed. Secondly, the cells were incubated with 20 nmol/L ERK inhibitor, and LPS was added for further stimulation. The changes in the above indexes were investigated. The relationship between the secretion of inflammatory cytokines and ERK signaling pathway was studied. The results showed that in normal RAW264.7 cells, LPS treatment stimulated the activation of ERK and secretion of TNF-α and IL-6 significantly, and had no significant effects on IL-10 level. CD36 knockdown inhibited the activation of ERK and secretion of TNF-α and IL-6, and increased IL-10 level upon LPS treatment. The pharmaceutical inhibition of ERK decreased TNF-α and IL-6 secretion and enhanced IL-10 secretion upon LPS treatment. The results suggest that both CD36 and ERK pathway are involved in LPS-mediated secretion of proinflammatory cytokines.
