Scutellarin Mitigates Aβ-Induced Neurotoxicity and Improves Behavior Impairments in AD Mice

Molecules. 2018 Apr 10;23(4):869. doi: 10.3390/molecules23040869.


Alzheimer's disease (AD) is pathologically characterized by excessive accumulation of amyloid-beta (Aβ) within extracellular spaces of the brain. Aggregation of Aβ has been shown to trigger oxidative stress, inflammation, and neurotoxicity resulting in cognitive dysfunction. In this study, we use models of cerebral Aβ amyloidosis to investigate anti-amyloidogenic effects of scutellarin in vitro and in vivo. Our results show that scutellarin, through binding to Aβ42, efficiently inhibits oligomerization as well as fibril formation and reduces Aβ oligomer-induced neuronal toxicity in cell line SH-SY5Y. After nine months of treatment in APP/PS1 double-transgenic mice, scutellarin significantly improves behavior, reduces soluble and insoluble Aβ levels in the brain and plasma, decreases Aβ plaque associated gliosis and levels of proinflammatory cytokines TNF-α and IL-6, attenuates neuroinflammation, displays anti-amyloidogenic effects, and highlights the beneficial effects of intervention on development or progression of AD-like neuropathology.

Keywords: APP/PS1 transgenic mice; Alzheimer’s disease (AD); Aβ-amyloid neurotoxicity; scutellarin.

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / psychology
  • Amyloid beta-Protein Precursor / blood
  • Amyloid beta-Protein Precursor / genetics
  • Amyloid beta-Protein Precursor / metabolism*
  • Animals
  • Apigenin / administration & dosage*
  • Apigenin / pharmacology
  • Brain / drug effects
  • Brain / metabolism
  • Cell Line
  • Cognitive Dysfunction / drug therapy*
  • Cognitive Dysfunction / metabolism
  • Disease Models, Animal
  • Female
  • Glucuronates / administration & dosage*
  • Glucuronates / pharmacology
  • Humans
  • Male
  • Mice
  • Treatment Outcome


  • Amyloid beta-Protein Precursor
  • Glucuronates
  • scutellarin
  • Apigenin