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

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 ox...

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Published inFood & function Vol. 9; no. 1; pp. 124 - 133
Main Authors Tu, Dom-Gene, Chang, Yao-Ling, Chou, Chung-Hsi, Lin, Yi-Ling, Chiang, Chia-Chun, Chang, Yuan-Yen, Chen, Yi-Chen
Format Journal Article
LanguageEnglish
Published England Royal Society of Chemistry 01.01.2018
Subjects
advanced glycation end products
Advanced glycosylation end products
antioxidant activity
Antioxidants
Apoptosis
Brain
Brain damage
Brain injury
CD11b antigen
cognition
Cognitive ability
D-Galactose
Damage prevention
Degeneration
Dentate gyrus
Galactose
Glial fibrillary acidic protein
Glycosylation
hippocampus
inflammation
Memory
Mice
Neurodegeneration
Neurodegenerative diseases
Oxidative stress
Searching
Shrinkage
Taurine
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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.
AbstractList 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.
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.
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.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.
Author Chiang, Chia-Chun
Chen, Yi-Chen
Tu, Dom-Gene
Lin, Yi-Ling
Chang, Yuan-Yen
Chang, Yao-Ling
Chou, Chung-Hsi
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  givenname: Yao-Ling
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  orcidid: 0000-0002-4616-2115
  surname: Chen
  fullname: Chen, Yi-Chen
  organization: Department of Animal Science and Technology, National Taiwan University, Taipei City 106, Taiwan, Zoonoses Research Center
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29068027$$D View this record in MEDLINE/PubMed
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  ident: C7FO01210A-(cit1)/*[position()=1]
– volume: 128
  start-page: 751
  year: 1998
  ident: C7FO01210A-(cit4)/*[position()=1]
  publication-title: J. Nutr.
  doi: 10.1093/jn/128.4.751
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Snippet Oxidative stress arising from life processes or environmental influences and its resultant cellular dysfunctions are major causes of neurodegenerative...
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StartPage 124
SubjectTerms advanced glycation end products
Advanced glycosylation end products
antioxidant activity
Antioxidants
Apoptosis
Brain
Brain damage
Brain injury
CD11b antigen
cognition
Cognitive ability
D-Galactose
Damage prevention
Degeneration
Dentate gyrus
Galactose
Glial fibrillary acidic protein
Glycosylation
hippocampus
inflammation
Memory
Mice
Neurodegeneration
Neurodegenerative diseases
Oxidative stress
Searching
Shrinkage
Taurine
Title Preventive effects of taurine against d -galactose-induced cognitive dysfunction and brain damage
URI https://www.ncbi.nlm.nih.gov/pubmed/29068027
https://www.proquest.com/docview/2010869394
https://www.proquest.com/docview/1955629396
https://www.proquest.com/docview/2220850825
Volume 9
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