出 处:《Biomedical and Environmental Sciences》2004年第1期79-86,共8页生物医学与环境科学(英文版)
基 金:This work was supported by a grant from the National Key Basic Research Development Program Foundation of China (No.G2000057010) ;a grant from the National Natural Science Foundation of China (No.30070827).
摘 要: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 respectively. Conclusion Enhanced levels of astrocytic oxidation stress and decrease of antioxidation abilities may contribute to, at least partially, the detrimental effects of AGEs in neuronal disorders and aging brain.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 respectively. Conclusion Enhanced levels of astrocytic oxidation stress and decrease of antioxidation abilities may contribute to, at least partially, the detrimental effects of AGEs in neuronal disorders and aging brain.
关 键 词:Advanced glycation end products ASTROCYTE Superoxide dismutase GLUTATHIONE MALONDIALDEHYDE MAO-B Nitric oxide
分 类 号:R741.02[医药卫生—神经病学与精神病学]
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