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 con...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.展开更多
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).
文摘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.
文摘目的研究羟基积雪草甙(madecassoside,MC)对慢性铝中毒痴呆小鼠的保护作用。方法葡萄糖酸铝按铝400 mg.kg-1.d-1灌胃90 d建立慢性铝中毒痴呆小鼠模型。通过HE染色、Morris水迷宫试验和生化实验,观察MC三种剂量(30、60和120 mg.kg-1.d-1)同步给药90d对小鼠海马神经元损伤、空间学习记忆能力和脑组织单胺氧化酶B(MAO-B)活性的影响。结果与模型组比较,30和60 mg.kg-1.d-1MC明显减轻铝过负荷所致的海马神经元损伤,明显缩短小鼠寻找平台潜伏期(s)(35.9±10.9 vs 16.5±8.4和19.6±10.5)(P<0.05);同时三种剂量MC均明显降低小鼠脑组织中MAO-B活性(U.h-1.mg-1prot)(18.9±1.8 vs 14.6±1.7,13.7±2.3和13.6±1.4)(P<0.05)。结论MC对慢性铝中毒小鼠海马神经元有保护作用,改善痴呆小鼠学习记忆能力。
