TY - JOUR
T1 - 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
AU - Tsai, Shih Jei
AU - Chiu, C. Perry
AU - Yang, Hui Ting
AU - Yin, Mei Chin
PY - 2011/6/8
Y1 - 2011/6/8
N2 - 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.
AB - 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.
KW - β-Amyloid
KW - glycation
KW - protein kinase C
KW - s-allyl cysteine
KW - s-ethyl cysteine
KW - s-propyl cysteine
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U2 - 10.1021/jf201160a
DO - 10.1021/jf201160a
M3 - Article
C2 - 21548553
AN - SCOPUS:79957979605
VL - 59
SP - 6319
EP - 6326
JO - Journal of Agricultural and Food Chemistry
JF - Journal of Agricultural and Food Chemistry
SN - 0021-8561
IS - 11
ER -