S-Allylcysteine prevents amyloid-β peptide-induced oxidative stress in rat hippocampus and ameliorates learning deficits

Pérez-Severiano, Francisca; Salvatierra-Sánchez, Raquel; Rodrı́guez-Pérez, Mayra; Cuevas-Martı́nez, Elvis Y; Guevara, Jorge; Limón, Daniel; Maldonado, Perla D.; Medina-Campos, Omar Noel; Pedraza‐Chaverrí, José; Santamarı́a, Abel

doi:10.1016/j.ejphar.2004.03.001

Cited by 76 publications

(33 citation statements)

References 25 publications

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“…Studies on cellular insults responsible for ER stress-induced cell death in human origin cells is also in progress in our laboratory. SAC, an organosulfur compound possessing a thioallyl group, present in AGE, has been shown to protect neurons against various toxic or ischemic conditions (7,21,35). Previous investigations in our laboratory have also shown that SAC protects NGF-differentiated PC12 cells (22) and cultured hippocampal neurons (3) against Aβ-and tunicamycin-induced toxicities.…”

Section: Discussionmentioning

confidence: 61%

Role of Caspase-12 in Amyloid β-Peptide-Induced Toxicity in Organotypic Hippocampal Slices Cultured for Long Periods

et al. 2007

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Abstract. Amyloid β (Aβ) toxicity has been implicated in cell death in the hippocampus, but its specific mechanisms are poorly understood. In this study, Aβ-induced cell death was investigated in organotypic hippocampal slice cultures (OHCs) that were cultured for various periods in vitro. There were no obvious histological differences among slices cultured for 3 to 7 weeks in vitro. Although there was little neurotoxicity after treatment with Aβ 25-35 in OHCs cultured for relatively shorter periods (3 -5 weeks), age-dependent cell death was evident in OHCs cultured for relatively longer periods (6 -7 weeks) after exposure to Aβ 25-35 . In OHCs cultured for 7 weeks, S-allyl-L-cysteine (SAC), a component of aged garlic extract, protected the cells in areas CA1 and CA3 and the dentate gyrus from Aβ 25-35 -induced toxicity. The immunoreactivity of cleaved caspase-12 was increased whereas that of glucose-regulated protein 78 was not altered after exposure to Aβ [25][26][27][28][29][30][31][32][33][34][35] . The increases in the cleaved caspase-12 were also reversed by simultaneously applied SAC. These results suggest that OHCs cultured for relatively longer periods are more susceptible to Aβ-induced toxicity and that the Aβ-induced cell death involves caspase-12-dependent pathways. It is also suggested that SAC is able to protect against the Aβ-induced neuronal cell death through the inhibition of the caspase-12-dependent pathway.

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Section: Discussionmentioning

confidence: 61%

Role of Caspase-12 in Amyloid β-Peptide-Induced Toxicity in Organotypic Hippocampal Slices Cultured for Long Periods

et al. 2007

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“…4,5) Furthermore, SAC also ameliorated learning deficits in senescence-accelerated mice, 6) evoked neurotrophic action, 7) and protected amyloid--induced neurotoxicity in hippocampal cultures. [8][9][10][11] Several studies have shown that improvements in nutritional factors are effective to prevent cerebral stroke and lengthen the life span in stroke-prone spontaneously hypertensive (SHRSP) rats. 12,13) Although SAC, known as a neuroprotectant, may possibly prevent cerebral stroke, the effect of dietary SAC on SHRSP is unknown.…”

mentioning

confidence: 99%

Dietary S-Allyl-L-cysteine Reduces Mortality with Decreased Incidence of Stroke and Behavioral Changes in Stroke-Prone Spontaneously Hypertensive Rats

Kim

Chang

Kim

et al. 2006

Bioscience, Biotechnology, and Biochemistry

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“…Oxidative stress caused by ROS is considered one of major causal factors of many neurodegenerative diseases. In rats, supplementation of SAC reduces amyloid beta (Aβ)-induced oxidative damage in the brain and improves cognitive function (PEREZ-SEVERIANO et al, 2004). The neuroprotective effect of SAC is further supported by a decrease in Aβ-induced apoptosis in hippocampal neurons (PENG et al, 2002).…”

Section: Introductionmentioning

confidence: 93%

Supplementation of S-allyl cysteine improves health span in Caenorhabditis elegans

Kim¹

2017

Biosci. J.

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Previous studies show that nutritional interventions with anti-oxidants have various healthpromoting effects in several model organisms. Here, we examine the effects of S-allyl cysteine on resistance to environmental stressors and age-related physiological changes using C. elegans as a model system. S-allyl cysteine is a modified amino acid found in aged garlic extracts and known to have strong anti-oxidant activity. The survival of worms under oxidative-stress conditions significantly increased with supplementation of S-allyl cysteine. In addition, pretreatment of S-allyl cysteine significantly increased resistance to both heat stress and ultraviolet irradiation. However, lifespan was not affected by S-allyl cysteine treatment. We also examined the effect of S-allyl cysteine on motility of C. elegans and found that S-allyl cysteine can retard the age-related decline of muscle tissue locomotive activity. S-allyl cysteine also significantly suppressed amyloid β-induced paralysis in Alzheimer's disease model animals. Taken together, our study indicates that dietary supplementation of S-allyl cysteine can improve health span and suggests that S-allyl cysteine can be used to develop novel health-promoting pharmaceuticals.

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S-Allylcysteine prevents amyloid-β peptide-induced oxidative stress in rat hippocampus and ameliorates learning deficits

Cited by 76 publications

References 25 publications

Role of Caspase-12 in Amyloid β-Peptide-Induced Toxicity in Organotypic Hippocampal Slices Cultured for Long Periods

Role of Caspase-12 in Amyloid β-Peptide-Induced Toxicity in Organotypic Hippocampal Slices Cultured for Long Periods

Dietary S-Allyl-L-cysteine Reduces Mortality with Decreased Incidence of Stroke and Behavioral Changes in Stroke-Prone Spontaneously Hypertensive Rats

Supplementation of S-allyl cysteine improves health span in Caenorhabditis elegans

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