Department of Nuclear Medicine, Ditmanson Medical Foundation, Chia-Yi Christian Hospital, Chia-Yi City 600, Taiwan.
Food Funct. 2018 Jan 24;9(1):124-133. doi: 10.1039/c7fo01210a.
Oxidative stress arising from life processes or environmental influences and its resultant cellular dysfunctions are major causes of neurodegenerative disorders. The objectives of this study were to investigate whether taurine (Tau) can prevent d-galactose-induced cognitive dysfunction and brain oxidative damage. Mice given with Tau supplementation (100 and 400 mg per kg BW per day) spent shorter (p < 0.05) time in searching target in d-galactose (100 mg per kg BW per day) treated mice in a water maze reference memory experiment. Moreover, Tau supplementation extended (p < 0.05) the searching period around the target quadrant in the probe test of the water maze, and neuronal degeneration and nucleus shrinkage in the hippocampus dentate gyrus area of d-galactose treated mice were observed to be attenuated. Tau also downregulated (p < 0.05) expression of the glial fibrillary acidic protein (Gfap) and of the cluster of differentiation marker Cd11b; meanwhile, it strengthened (p < 0.05) antioxidant capacity and lowered (p < 0.05) the accumulation of advanced glycation end-products (AGEs) in the brain. Therefore, Tau could be effective to ameliorate oxidative damage and inflammation in the brain, and apoptosis of brain cells, which further lessen the cognitive dysfunction.
氧化应激是由生命过程或环境影响引起的，其导致的细胞功能障碍是神经退行性疾病的主要原因。本研究的目的是探讨牛磺酸（Tau）是否能预防半乳糖诱导的认知功能障碍和大脑氧化损伤。在水迷宫参考记忆实验中，给予 Tau 补充剂（100 和 400 mg/kg BW/天）的小鼠在半乳糖（100 mg/kg BW/天）处理的小鼠中搜索目标的时间更短（p<0.05）。此外，Tau 补充剂延长了（p<0.05）在水迷宫探针测试中搜索目标象限的时间，并且观察到半乳糖处理的小鼠海马齿状回区的神经元变性和细胞核收缩减轻。Tau 还下调（p<0.05）了神经胶质纤维酸性蛋白（Gfap）和分化标志物 Cd11b 的表达；同时，它增强了（p<0.05）了大脑的抗氧化能力，降低了（p<0.05）了晚期糖基化终产物（AGEs）的积累。因此，Tau 可能有效改善大脑氧化损伤和炎症、以及脑细胞凋亡，从而减轻认知功能障碍。
