S-allyl cysteine, s-ethyl cysteine, and s -propyl cysteine alleviate β-amyloid, glycative, and oxidative injury in brain of mice treated by d -galactose

Shih Jei Tsai, C. Perry Chiu, Hui Ting Yang, Mei Chin Yin

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

The neuroprotective effects of s-allyl cysteine, s-ethyl cysteine, and s-propyl cysteine in d-galactose (DG)-treated mice were examined. DG treatment increased the formation of Aβ1-40 and Aβ1-42, enhanced mRNA expression of β-amyloid precursor protein (APP) and β-site APP cleavage enzyme 1 (BACE1), and reduced neprilysin expression in brain (P < 0.05); however, the intake of three test compounds significantly decreased the production of Aβ1-40 and Aβ1-42 and suppressed the expression of APP and BACE1 (P < 0.05). DG treatments declined brain protein kinase C (PKC) activity and mRNA expression (P < 0.05). Intake of test compounds significantly retained PKC activity, and the expression of PKC-α and PKC-γ (P < 0.05). DG treatments elevated brain activity and mRNA expression of aldose reductase (AR) and sorbitol dehydrogenase as well as increased brain levels of carboxymethyllysine (CML), pentosidine, sorbitol, and fructose (P < 0.05). Test compounds significantly lowered AR activity, AR expression, and CML and pentosidine levels (P < 0.05). DG treatments also significantly increased the formation of reactive oxygen species (ROS) and protein carbonyl and decreased the activity of glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase (P < 0.05); however, the intake of test compounds in DG-treated mice significantly decreased ROS and protein carbonyl levels and restored brain GPX, SOD, and catalase activities (P < 0.05). These findings support that these compounds via their anti-Aβ, antiglycative, and antioxidative effects were potent agents against the progression of neurodegenerative disorders such as Alzheimer's disease.

Original languageEnglish
Pages (from-to)6319-6326
Number of pages8
JournalJournal of Agricultural and Food Chemistry
Volume59
Issue number11
DOIs
Publication statusPublished - Jun 8 2011
Externally publishedYes

Fingerprint

amyloid
Galactose
Amyloid
galactose
Brain Injuries
Cysteine
cysteine
Brain
protein kinase C
aldehyde reductase
brain
Aldehyde Reductase
Amyloid beta-Protein Precursor
mice
pentosidine
Protein Kinase C
Glutathione Peroxidase
proteins
glutathione peroxidase
Catalase

Keywords

  • β-Amyloid
  • glycation
  • protein kinase C
  • s-allyl cysteine
  • s-ethyl cysteine
  • s-propyl cysteine

ASJC Scopus subject areas

  • Chemistry(all)
  • Agricultural and Biological Sciences(all)

Cite this

S-allyl cysteine, s-ethyl cysteine, and s -propyl cysteine alleviate β-amyloid, glycative, and oxidative injury in brain of mice treated by d -galactose. / Tsai, Shih Jei; Chiu, C. Perry; Yang, Hui Ting; Yin, Mei Chin.

In: Journal of Agricultural and Food Chemistry, Vol. 59, No. 11, 08.06.2011, p. 6319-6326.

Research output: Contribution to journalArticle

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abstract = "The neuroprotective effects of s-allyl cysteine, s-ethyl cysteine, and s-propyl cysteine in d-galactose (DG)-treated mice were examined. DG treatment increased the formation of Aβ1-40 and Aβ1-42, enhanced mRNA expression of β-amyloid precursor protein (APP) and β-site APP cleavage enzyme 1 (BACE1), and reduced neprilysin expression in brain (P < 0.05); however, the intake of three test compounds significantly decreased the production of Aβ1-40 and Aβ1-42 and suppressed the expression of APP and BACE1 (P < 0.05). DG treatments declined brain protein kinase C (PKC) activity and mRNA expression (P < 0.05). Intake of test compounds significantly retained PKC activity, and the expression of PKC-α and PKC-γ (P < 0.05). DG treatments elevated brain activity and mRNA expression of aldose reductase (AR) and sorbitol dehydrogenase as well as increased brain levels of carboxymethyllysine (CML), pentosidine, sorbitol, and fructose (P < 0.05). Test compounds significantly lowered AR activity, AR expression, and CML and pentosidine levels (P < 0.05). DG treatments also significantly increased the formation of reactive oxygen species (ROS) and protein carbonyl and decreased the activity of glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase (P < 0.05); however, the intake of test compounds in DG-treated mice significantly decreased ROS and protein carbonyl levels and restored brain GPX, SOD, and catalase activities (P < 0.05). These findings support that these compounds via their anti-Aβ, antiglycative, and antioxidative effects were potent agents against the progression of neurodegenerative disorders such as Alzheimer's disease.",
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