Preventive effects of taurine against D-galactose-induced cognitive dysfunction and brain damage

doi:10.1039/c7fo01210a

CNU IR > Pharmacy and Science > Dept. of Food Science & Technology > Periodical Articles > Item 310902800/32271

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/32271

Title:	Preventive effects of taurine against D-galactose-induced cognitive dysfunction and brain damage
Authors:	Tu, Dom-Gene Chang, Yao-Ling Chou, Chung-Hsi Lin, Yi-Ling Chiang, Chia-Chun Chang, Yuan-Yen Chen, Yi-Chen
Contributors:	Chia Yi Christian Hosp, Ditmanson Med Fdn, Dept Nucl Med Chia Nan Univ Pharm & Sci, Dept Food Sci & Technol Chang Jung Christian Univ, Coll Hlth Sci Natl Taiwan Univ, Dept Anim Sci & Technol Natl Taiwan Univ, Sch Vet Med Natl Taiwan Univ, Zoonoses Res Ctr Chung Jen Jr Coll Nursing Hlth Sci & Management, Dept Nursing Chung Shan Med Univ, Sch Med, Dept Microbiol & Immunol Chung Shan Med Univ Hosp, Clin Lab
Keywords:	Oxidative Stress Advanced Glycation Aging Model Mouse Model Rats Impairment Memory Acid Inflammation Apoptosis
Date:	2018-01
Issue Date:	2019-11-15 15:47:37 (UTC+8)
Publisher:	ROYAL SOC CHEMISTRY
Abstract:	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.
???metadata.dc.relation.uri???:	http://dx.doi.org/10.1039/c7fo01210a
Relation:	Food & Function, v.9, n.1, pp.124-133
Appears in Collections:	[Dept. of Food Science & Technology] Periodical Articles

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