Abstract: The role of p-ERK1/2 in nitric oxide induced cell apoptosis was investigated in this paper.Human hepatoma cells HepG2 were treated by sodium nitroprusside (SNP) in a dose-dependent manner with a control group.The amount of nitric oxide produced by SNP was determined by NO-DAF technique and Griess assay,respectively.Apoptosis of HepG2 cells was detected by flow cytometry and the level of p-ERK1/2 expression was determined by Western blot assay.Mutated ERK1 plasmid was constructed according to the handbook of site-directed gene mutagenesis kit and the plasmids were transfected by Lipofectamine 2000 reagent.Results showed 1 mmol/L SNP could effectively induce HepG2 cell apoptosis with increasing p-ERK1/2 expression and nitric oxide concentrations compared with the control group.Furthermore,pre-treatment of NO scavenger hemoglobin (HB) notably reduced the concentrations of nitric oxide and inhibited SNP induced cell apoptosis and activation of ERK1/2.Overexpression of dominate positive ERK1 plasmid which can phosphorylate PPARγ increased SNP induced cell apoptosis.These results suggest nitric oxide could induce cell apoptosis by up regulating the expression of p-ERK1/2,which implies the important role of p-ERK1/2 in nitric oxide induced cell apoptosis,and may shed a new light on the discovery of relevant mechanisms.