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Silibinin: a novel inhibitor of Aβ aggregation
Fei Yin1, Jianhui Liu, Xiuhong Ji
1Research Center of Medicinal Chemistry and Chemical Biology, Chongqing Technology and Business University, Chongqing, 400067, PR China.
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 Aβ(1-42)-induced oxidative stress by decreasing H(2)O(2) production in Aβ(1-42)-stressed neurons. Taken together, these results indicate that silibinin may be a novel therapeutic agent for the treatment of AD.
Insights
Silibinin, a compound from milk thistle, inhibits amyloid-beta aggregation and reduces neurotoxicity, offering a potential new treatment for Alzheimer's disease (AD). This discovery highlights silibinin's therapeutic promise for AD.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Alzheimer's disease (AD) is linked to amyloid-beta (Aβ) plaque formation.
- Inhibiting Aβ aggregation is a key therapeutic strategy for AD.
- Silibinin's effects on Aβ neurotoxicity require further investigation.
Purpose of the Study:
- To investigate if silibinin directly inhibits Aβ aggregation.
- To determine if silibinin reduces Aβ-induced neurotoxicity.
- To explore silibinin as a potential Alzheimer's disease therapeutic.
Main Methods:
- Thioflavin T (ThT) assay to monitor Aβ aggregation.
- Electron microscopy to visualize Aβ fibril formation.
- Cell-based assays using SH-SY5Y cells to assess oxidative stress and H(2)O(2) production.
Main Results:
- Silibinin demonstrated dose-dependent inhibition of Aβ aggregation.
- Electron microscopy confirmed silibinin's effect on Aβ fibril formation.
- Silibinin protected SH-SY5Y cells from Aβ(1-42)-induced oxidative stress by reducing H(2)O(2) levels.
Conclusions:
- Silibinin acts as a novel inhibitor of Aβ aggregation.
- Silibinin mitigates Aβ-induced neurotoxicity and oxidative stress.
- Silibinin shows potential as a therapeutic agent for Alzheimer's disease treatment.
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