Cycloastragenol inhibits Aβ1-42-induced blood-brain barrier disruption and enhances soluble Aβ efflux in vitro

J Asian Nat Prod Res. 2021 Jun;23(6):556-569. doi: 10.1080/10286020.2020.1786372. Epub 2020 Jul 1.

Abstract

This study aimed to evaluate the effect Cycloastragenol (CAG), a triterpenoid saponin isolated from the Radix astragali, on Aβ-induced BBB damage. An immortalized endothelial cell line (bEnd.3) was employed to mimic a BBB. The Western blot, TUNEL staining, Flow cytometric analysis and Enzyme-linked immunosorbent assay were performed. The present results showed that CAG (10, 50, 75 μM) can alleviate oligomer Aβ1-42 induced bEnd.3 cell apoptosis and increase tight junction scaffold proteins expression. The result also indicated that CAG increased soluble Aβ efflux across BBB via upregulation of the P-gp and downregulation of RAGE expression.[Formula: see text].

Keywords: Alzheimer's disease; amyloid‐β1–42; blood–brain barrier; cycloastragenol.

MeSH terms

  • Amyloid beta-Peptides* / metabolism
  • Animals
  • Blood-Brain Barrier* / drug effects
  • Blood-Brain Barrier* / metabolism
  • Cell Line
  • Mice
  • Molecular Structure
  • Peptide Fragments
  • Sapogenins / pharmacology*

Substances

  • Amyloid beta-Peptides
  • Peptide Fragments
  • Sapogenins
  • amyloid beta-protein (1-42)
  • cycloastragenol