2011
DOI: 10.1021/jf201160a
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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

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 Aβ(1-40) and Aβ(1-42), 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 Aβ(1-40) and Aβ(1-42) and suppressed the expression of APP and BACE1 (… Show more

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Cited by 44 publications
(26 citation statements)
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References 32 publications
(52 reference statements)
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“…The CML formations in the ELISA data (Figure 2(C)) were comparable to those of the immune stains (Figure 2(B)) in Western blotting. The D -glc or D -gal was reported to react with proteins/peptides both in vitro and in vivo , as well as with their metabolized intermediates such as glyoxal or MGO, leading to AGE formations through nonenzymatic glycation (Song et al 1999;Parameshwaran et al 2010;Tsai et al 2011). The reaction rate of D -gal is approximately 4.7-fold of the reactivity of D -glc toward hemoglobin in vitro (Burn and Higgins 1981).…”
Section: Resultsmentioning
confidence: 99%
“…The CML formations in the ELISA data (Figure 2(C)) were comparable to those of the immune stains (Figure 2(B)) in Western blotting. The D -glc or D -gal was reported to react with proteins/peptides both in vitro and in vivo , as well as with their metabolized intermediates such as glyoxal or MGO, leading to AGE formations through nonenzymatic glycation (Song et al 1999;Parameshwaran et al 2010;Tsai et al 2011). The reaction rate of D -gal is approximately 4.7-fold of the reactivity of D -glc toward hemoglobin in vitro (Burn and Higgins 1981).…”
Section: Resultsmentioning
confidence: 99%
“…D-Galactose induces AD-like pathological changes in the brain, including increased reactive oxygen species, decreased antioxidant enzyme activity, and enhanced A β -peptide expression. SAC decreased the brain levels of A β 1–40 and A β 1–42 , lowered amyloid precursor protein level and BACE1 expressions and activities (both of them being factors responsible for A β accumulation and AD progression), retained PKC activity and expression of PKC- α and PKC- γ , lowered A β accumulation, reduced the levels of advanced glycation end products (carboxymethyllysine, pentosidine), lowered aldose reductase activity and expression (an enzyme that facilitates the production of sorbitol and fructose, which in turn promote advanced glycation end products formation and glycative stress), and displayed antioxidant protection (evidenced by increased reduced glutathione content and glutathione peroxidase, superoxide dismutase, and catalase activities, accompanied by decreased levels of malondialdehyde, reactive oxygen species, and protein carbonyls) [105]. …”
Section: Neuroprotective Effects Of Sacmentioning
confidence: 99%
“…(33,34) Based on these findings, these compounds could be potent agents against the progression of neurodegenerative disorders, such as Alzheimer’s disease, via their anti-amyloid beta, antiglycative, and antioxidative effects respectively. DJ-1 and Cu/Zn-SOD are both tightly connected to the Nrf2 protein, which is a transcription factor and master regulator for the expression of many antioxidant/detoxification genes.…”
Section: Discussionmentioning
confidence: 99%