Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10958334 | Neurochemistry International | 2011 | 5 Pages |
Abstract
Alzheimer's disease (AD) is characterized by the abnormal aggregation of amyloid β peptide (Aβ) into extracellular fibrillar deposits known as amyloid plaque. Inhibition of Aβ aggregation is therefore viewed as a potential method to halt or slow the progression of AD. It is reported that silibinin (silybin), a flavonoid derived from the herb milk thistle (Silybum marianum), attenuates cognitive deficits induced by Aβ25-35 peptide and methamphetamine. However, it remains unclear whether silibinin interacts with Aβ peptide directly and decreases Aβ peptide-induced neurotoxicity. In the present study, we identified, through employing a ThT assay and electron microscopic imaging that silibinin also appears to act as a novel inhibitor of Aβ aggregation and this effect showed dose-dependency. We also show that silibinin prevented SH-SY5Y cells from injuries caused by Aβ1-42-induced oxidative stress by decreasing H2O2 production in Aβ1-42-stressed neurons. Taken together, these results indicate that silibinin may be a novel therapeutic agent for the treatment of AD.
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Authors
Fei Yin, Jianhui Liu, Xiuhong Ji, Yanwen Wang, Jeffrey Zidichouski, Junzeng Zhang,