Advanced glycation end products (AGEs), a group of complex compounds generated by nonenzymatic interactions between amino acids, proteins and reducing sugars or lipids, accumulate in vivo and activate various signaling pathways closely related to the occurrence of various chronic metabolic diseases. This study aims to explore the structure-activity relationship between phenolic acids with different structure and affecting the AGEs generation, and to provide data support for AGEs control. Phenolic acids (4-hydroxybenzoic, protocatechuic, gallic, p-coumaric, caffeic, ferulic and sinapic acids) were employed to indicate the AGEs formation condition in Maillard reaction performed in the glucose-lysine model system. Three 1,2-dicarbonyl compounds were reacted with phenolic acids and then tested by liquid chromatography-mass spectrometry. The results showed that Nε-carboxy-methyl-lysine (CML), Nε-carboxy-ethyl-lysine (CEL), and pyrraline formation inhibited by phenolic acids varied from (8.7 ± 2.5)% to (33.2 ± 2.5)%, (10.5 ± 0.8)% to (57.1 ± 3.2)% and (1.3 ± 0.3)% to (23.3 ± 0.8)%, respectively. The p-coumaric acid has no inhibitory effect on CML and CEL formation. Gallic acid shows the best inhibitory effect on CML formation due to its strong antioxidant activity. Sinapic acid showed the best glyoxal (GO) trapping rate and thus had the stronger inhibitory effect on CML formation. Ferulic acid can react with mono-, di-, and tri-methylglyoxal (MGO) to form adduct products, showing the best MGO scavenging rate and a good inhibitory effect on CEL formation. The main role of phenolic acid is an antioxidant agent to inhibit pyrraline formation. The glucose itself or ammonia-induced degradation and Amadori rearrangement products oxidation were lowered by protocatechuic, gallic and caffeic acids due to their antioxidant activities to form AGEs, while AGEs inhibited by ferulic and sinapic acids were mainly dependent on their trapping ability on 1,2-dicarbonyl compounds.