3,6'-Disinapoylsucrose alleviates the amyloid precursor protein and lipopolysaccharide induced cognitive dysfunction through upregulation of the TrkB/BDNF pathway

J Asian Nat Prod Res. 2023 Apr;25(4):387-402. doi: 10.1080/10286020.2022.2069565. Epub 2022 Jun 7.

Abstract

The aim of this study is to explore the effect and mechanism of 3,6'-disinapoylsucrose (DISS) on an Alzheimer's disease (AD) mice model induced by APPswe695 lentivirus (LV) and intraperitoneal injection of lipopolysaccharide (LPS). The results show that DISS improves cognitive ability, decreases the levels of IL-2, IL-6, IL-1β, and TNF-α, reduces the expression of NF-κB p65, and alleviates Aβ deposition and nerve cell damage. DISS can regulate tyrosine kinase B (TrkB)/brain-derived neurotrophic factor (BDNF) signaling in the hippocampus. In summary, DISS can significantly alleviate neuroinflammation, spatial learning and memory disorders in AD model mice.

Keywords: Alzheimer's disease; BDNF; LPS; TrkB; neuroinflammation.

MeSH terms

  • Alzheimer Disease* / metabolism
  • Amyloid beta-Peptides / metabolism
  • Amyloid beta-Protein Precursor / metabolism
  • Amyloid beta-Protein Precursor / pharmacology
  • Animals
  • Brain-Derived Neurotrophic Factor / metabolism
  • Brain-Derived Neurotrophic Factor / pharmacology
  • Cognitive Dysfunction* / metabolism
  • Hippocampus / metabolism
  • Lipopolysaccharides / pharmacology
  • Mice
  • Protein-Tyrosine Kinases / metabolism
  • Protein-Tyrosine Kinases / pharmacology
  • Up-Regulation

Substances

  • Protein-Tyrosine Kinases
  • Amyloid beta-Protein Precursor
  • Brain-Derived Neurotrophic Factor
  • Lipopolysaccharides
  • 3,6'-disinapoylsucrose
  • Amyloid beta-Peptides