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Methylglyoxal (MGO) are formed under hyperglycemic conditions and behave as advanced glycation end products (AGEs) precursors.It forms adducts on proteins, thereby inducing cellular dysfunctions involved in chronic complications of diabetes.N(ε)-carboxymethyl-lysine (CML) and N(ε)-carboxyethyl-lysine (CEL) are the major AGE adducts formed from GO and MGO, respectively.To establish a CEL formation model, MGO is incubated with cultured endothelial cells (EA.hy926 Cell) and CEL formation is measured as fluorescence intensity by immunofluorescence.In present research, we found MGO less than 1mM will not cause a significant cytotoxicity.Concentration of upon 50 μM MGO will induce significant compared with control group, and there is no significant difference between the 50 μM, 100 μM, 200 μM, 400 μM and 800 μM group.However, 100 μM MGO induced CEL formation can be inhibited EGCG with a ratio of 1:1 by if MGO is premixed with EGCG 1h before incubation.The inhibition rate of EGCG premixed group has no significant difference with that of 100 μM aminoguanidine.We demonstrated that EGCG inhibit the formation of CEL induced by MGO in cultured endothelial cells.Furthermore, MGO induced cytotoxicity maybe inhibited by EGCG via inhibiting reactive oxygen species production.The results of this study indicate that EGCG is a potentially novel candidate for the treatment of atherosclerosis.