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sesaminol/amiloidosis

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Effect of sesaminol glucosides on beta-amyloid-induced PC12 cell death through antioxidant mechanisms.

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Several lines of evidence support that beta-amyloid (Abeta)-induced neurotoxicity is mediated through the generation of reactive oxygen species (ROS) and elevation of intracellular calcium. In this study, we have investigated protective effects of sesaminol glucosides on Abeta-induced oxidative cell

Sesaminol glucosides protect beta-amyloid peptide-induced cognitive deficits in mice.

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This study was designed to investigate the effect of sesaminol glycosides (SG), one of the most abundant lignan glycosides in sesame (Sesamum indicum LINN.) seed, on cognitive deficits and oxidative stress induced by intracerebroventricular (i.c.v.) injection of beta-amyloid protein (Abeta)(25-35)

Sesaminol glucosides protect β-amyloid induced apoptotic cell death by regulating redox system in SK-N-SH cells.

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We have investigated the neuroprotective effect of sesaminol glucosides (SG) in SK-N-SH cells. SG prevented apoptotic cell death induced by Aβ₂₅₋₃₅. In parallel, SK-N-SH cells exposed to Aβ₂₅₋₃₅ underwent oxidative stress as shown by the elevated level of intracellular ROS, lipid peroxidation, and

Effects of Sesaminol Feeding on Brain Aβ Accumulation in a Senescence-Accelerated Mouse-Prone 8.

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Alzheimer's disease (AD) is characterized by the progressive accumulation of extracellular β-amyloid (Aβ) aggregates. Recently, the senescence-accelerated mouse-prone 8 (SAMP8) model was highlighted as a useful model of age-related AD. Therefore, we used the SAMP8 mouse to investigate the preventive
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