本研究以鼠源巨噬细胞RAW264.7为模型，研究CD36和胞外信号调节激酶(ERK)通路对脂多糖(LPS)诱导巨噬细胞分泌炎症因子的影响。首先用100 ng/ml LPS刺激正常及小干扰RNA(siRNA)技术沉默CD36表达的巨噬细胞16 h，检测巨噬细胞的ERK活性及分泌炎症因子如肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)和IL-10的水平；继而以20 nmol/L ERK抑制剂处理细胞，再用LPS刺激，检测以上各项指标的变化，进一步明确ERK通路与LPS诱导巨噬细胞分泌炎症因子的相关性。结果显示，经LPS刺激，巨噬细胞的ERK活性显著增强，分泌的促炎因子TNF-α和IL-6显著增高，抑炎因子IL-10水平无明显变化；与CD36正常表达的巨噬细胞相比，CD36表达下降的巨噬细胞ERK活性及促炎因子TNF-α、IL-6水平显著下降，抑炎因子IL-10显著增多。与未处理组相比，ERK抑制剂预处理的巨噬细胞中LPS诱导的ERK活性显著降低，促炎因子TNF-α和IL-6水平降低，抑炎因子IL-10水平升高。结果提示，LPS能通过其受体——CD36，激活巨噬细胞内ERK活性，进而促进巨噬细胞促炎因子的分泌。

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.