Silibinin: a novel inhibitor of Aβ aggregation

Neurochem Int. 2011 Feb;58(3):399-403. doi: 10.1016/j.neuint.2010.12.017. Epub 2010 Dec 24.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / metabolism
  • Amyloid beta-Peptides / antagonists & inhibitors*
  • Amyloid beta-Peptides / metabolism
  • Amyloid beta-Peptides / poisoning
  • Antioxidants / pharmacology*
  • Antioxidants / therapeutic use
  • Cell Line, Tumor
  • Humans
  • Neuroprotective Agents / pharmacology*
  • Neuroprotective Agents / therapeutic use
  • Plaque, Amyloid / drug therapy*
  • Plaque, Amyloid / metabolism
  • Silybin
  • Silymarin / pharmacology*
  • Silymarin / therapeutic use


  • Amyloid beta-Peptides
  • Antioxidants
  • Neuroprotective Agents
  • Silymarin
  • Silybin