Objective To study the effects of propofol on the lipopolysaccharide induced activation of mitogen-activated protein kinase(MAPK) pathway in human mononuclear macrophage cells(THP-1). Methods Cultured THP-1 cells were randomly divided into four groups: intralipid(the solvent for propofol, 20 mg/L) group (C group), LPS(10 mg/L) group (L group), propofol(20 mg/L) group (P group), propofol(20 mg/L) and LPS(10 mg/L) group (P+L group). The phosphorylation of p38MAPK, extracellular-signal regulated protein kinase(ERK)1/2 and c-Jun amino-terminal kinase(JNK)1/2 were detected by western blot assay at 0.5, 1, 2 h and 6 h after LPS or propofol treatment. Results Compared with C group, the level of p-p38MAPK(relative intensity: 14.67±0.82), p-ERK1/2(relative intensity: 1.34±0.05) and p-JNK1/2(relative intensity: 4.49±0.51) increased dramatically in L group at 0.5 h after LPS treatment(P＜0.05). Compared with C group, the level of p-p38MAPK(relative intensity:11.78±0.75), p-ERK1/2(relative intensity: 0.58±0.05) and p-JNK1/2(relative intensity: 3.31±0.55) in L group increased significantly at 1h after LPS treatment(P＜0.05). However, the phosphorylation level of p-ERK1/2(relative intensity: 0.14±0.02) in P+L group was significantly lower than that of L group at 1 h. After LPS treatment 2 h, compared with C group the level of p-p38MAPK(relative intensity: 15.60±0.96) and p-JNK1/2(relative intensity: 8.33±0.70) in L group increased obviously(P＜0.05), but compared with L group, the level of p-p38MAPK(relative intensity: 4.52±0.23), p- JNK1/2(relative intensity: 1.80±0.70) decreased dramatically in P+L group(P＜0.05). After LPS treatment 6 h, the level of p-p38MAPK(relative intensity: 18.89±1.22) and p-JNK1/2(relative intensity: 2.58±0.50) increased significantly in L group(P＜0.05) compared with C group, however, the phosphorylation level of p38MAPK(relative intensity: 3.91±0.30) in P+L group was obviously lower than that of L group(P＜0.05). Conclusions In THP-1 cells, LPS can induce the phosphorylation of p38MAPK, ERK1/2 and JNK1/2, however, this effect can be partial inhibited by propofol, with might be the potential mechanism in anti-inflammation effect.