Aim To demonstrate the activation and nuclear translocation of the nuclear factor-κB（NF-κB） induced by advanced glycation end products （AGEs） in human dermal microvascular endothelial cells （HDMECs） , and to elucidate the roles of oxidative stress and endoplasmic reticulum stress in this pathological procedure. Methods HDMECs were incubated with AGEs-modified bovine serum albumin （AGE-BSA） at concentration of 100 mg/L for 1 h. As control, BSA of the same concentration was administered to HDMECs. NF-κB nuclear translocation was observed by immunofluorescent staining. Subsequently, HDMECs were pretreated with reduced glutathione （GSH）, apocynin, a pharmacological inhibitor of NADPH oxidase （NOX）, NOX4 siRNA or inositol requiring enzyme 1α （IRE1α） siRNA, and then administrated with AGE-BSA for 1 h. Changes of NF-κB nuclear translocation was observed. Results The results demonstrated the translocation of NF-κB from the cytoplasm to the nucleus upon the stimulation of AGE-BSA. Inhibition of reactive oxygen species generation with GSH or apocynin greatly attenuated these responses. Transfection of NOX4-small interfering RNA or IRE1α-small interfering RNA in HDMECs also significantly attenuated the AGE-induced translocation of NF-κB. Conclusion Oxidative stress and endoplasmic reticulum stress are possibly involved in the mediation of AGE-induced activation of NF-κB in endothelial cells.