Abstract
Background: The oxidative stress produced from life or environment and its resultant cellular dysfunctions are major causes of neurodegenerative disorders. The objectives of this study were to investigate if taurine (Tau) can prevent D-galactose-induced cognitive dysfunction and brain oxidative damages.
Methods: 45 mice were randomly divided into five groups: (1) Control (CON): 0.3-mL saline and 0.2-mL distilled water (oral gavage); (2) DG: 100 mg D-galactose/kg BW in 0.3-mL saline and 0.2-mL distilled water (oral gavage); (3) DG_LT: 100 mg D-galactose/kg BW in 0.3-mL saline and 100 mg Tau/kg BW in 0.2-mL distilled water (oral gavage); (4) DG_HT: 100 mg D-galactose/kg BW in 0.3-mL saline and 400 mg Tau/kg BW in 0.2-mL distilled water (oral gavage); (5) DG_AG: 100 mg D-galactose/kg BW in 0.3-mL saline and 50 mg aminoguanidine hydrochloride/kg BW in 0.2-mL distilled water (oral gavage) for 9 weeks. Learning and memory behavioral tests (Morris water maze: reference memory and probe tasks), histological analysis of hippocampus, and possible molecular protective mechanism in brains were investigated in this study.
Results: Tau supplementation spent shorter (p<0.05) time in searching target in D-galactose treated mice in a water maze reference memory experiment. Meanwhile, Tau supplementation extended (p<0.05) the searching period around target quadrant in the probe test of water maze while neuronal degeneration and nucleus shrinkage in hippocampus dentate gyrus area of D-galactose treated mice were attenuated. Tau also downregulated (p<0.05) expressions of glial fibrillary acidic protein (Gfap) and cluster of differentiation marker Cd11b; meanwhile, strengthened (p<0.05) the antioxidant capacity and lowered (p<0.05) advanced glycation end-products (AGEs) accumulation in brains.
Conclusion: 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.
