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The resveratrol trimer miyabenol C inhibits β-secretase activity and β-amyloid generation

Jin Hu1, Ting Lin2, Yuehong Gao3

  • 1Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, School of Pharmaceutical Sciences, Xiamen University, Xiamen, 361102, China; Institute of Neuroscience, College of Medicine, Xiamen University, Xiamen, 361102, China.

Plos One
|January 29, 2015
PubMed

Insights

Miyabenol C, derived from Vitis thunbergii, effectively reduces amyloid-beta (Aβ) in Alzheimer

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) pathogenesis is linked to amyloid-beta (Aβ) peptide accumulation.
  • Aβ is produced via sequential cleavage of amyloid-beta precursor protein (APP) by β-secretase and γ-secretase.
  • Inhibiting β-secretase is a key therapeutic strategy for AD.

Purpose of the Study:

  • To investigate the potential of miyabenol C, a resveratrol trimer from Vitis thunbergii, as a therapeutic agent for Alzheimer's disease.
  • To elucidate the mechanism by which miyabenol C affects Aβ production.

Main Methods:

  • Cell cultures and AD model mice were used to assess Aβ and sAPPβ levels.
  • Western blotting and enzyme activity assays were employed to study protein levels and secretase activity.
  • In vitro and in vivo assays were conducted to evaluate β-secretase inhibition.

Main Results:

  • Miyabenol C significantly reduced Aβ and sAPPβ levels in both cell cultures and AD model mice.
  • Miyabenol C did not alter the protein levels of APP, ADAM10, TACE, Presenilin 1, or affect γ-secretase-mediated Notch processing and TACE activity.
  • Miyabenol C inhibited both in vitro and in vivo β-secretase activity without affecting BACE1 protein levels.

Conclusions:

  • Miyabenol C acts as a potent β-secretase inhibitor.
  • Miyabenol C demonstrates potential as a lead compound for Alzheimer's disease drug development.

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