Objective To investigate whether two kinds of in vitro prepared advanced glycation end products (AGEs), Glu-BSA and Gal-BSA, could change oxidation stress and anti-oxidation abilities in astrocytes, and thus might contribute to brain injury. Methods Changes of GSH, MDA, SOD, MAO-B, nitric oxide were measured after AGEs treatment. Results Both 0.1 g/L Glu-BSA and Gal-BSA could slightly decrease GSH level, while 1 g/L of them significantly decreased GSH level by 35% and 43% respectively. The MDA levels of both 1 g/L AGEs treated groups (306±13 and 346±22) were higher than that of the normal group (189±18), which could be inhibited by free radical scavenger NAC. The SOD activities of both 1 g/L AGEs treated groups (67.0±5.2 and 74.0±11.0) were lower than that of the normal group (85.2±8.0). Both 0.1 g/L AGEs could slightly increase the activity of MAO-B, while 1 g/L of them could increase MAO-B activity by 1.5 and 1.7 folds respectively. Both AGEs stimulation could produce NO level by 1.7 and 2 folds Objective To investigate whether two kinds of in vitro advanced glycation end products (AGEs), Glu-BSA and Gal-BSA, could change oxidation stress and anti-oxidation abilities in astrocytes, and thus might contribute to brain injury. Methods Changes in GSH Results showed that both 0.1 g / L Glu-BSA and Gal-BSA could slightly decrease GSH level while 1 g / L of them significantly reduced GSH level by 35% the MDA levels of both 1 g / L AGEs treated groups (306 ± 13 and 346 ± 22) were higher than that of the normal group (189 ± 18), which could be inhibited by free radical scavenger NAC. The SOD activities of both 1 g / L AGEs treated groups (67.0 ± 5.2 and 74.0 ± 11.0) were lower than those of the normal group (85.2 ± 8.0). Both 0.1 g / L AGEs could slightly increase the activity of MAO-B , while 1 g / L of them could increase MAO-B activity by 1.5 and 1.7 folds respectively. Both AGEs stimulation could produce NO level by 1.7 and 2 folds