Cognitive-enhancing and ameliorative effects of acanthoside B in a scopolamine-induced amnesic mouse model through regulation of oxidative/inflammatory/cholinergic systems and activation of the TrkB/CREB/BDNF pathway

Food Chem Toxicol. 2019 Jul:129:444-457. doi: 10.1016/j.fct.2019.04.062. Epub 2019 May 8.

Abstract

Recently, our research team reported the anti-amnesic potential of desalted-hydroethanolic extracts of Salicornia europaea L. (SE-EE). In this study, we performed bioactivity-guided isolation and identification of Acanthoside B (Aca.B), from SE-EE, as the potential bioactive candidate and examined anti-amnesic activity with its potential mechanism of action using an in vivo model. S7-L3-3 purified from SE-EE showed enhanced in vitro acetylcholinesterase (AChE) inhibitory activity. The isolated S7-L3-3 was identified and characterized as Aca.B using varied spectral analyses, i.e., Nuclear magnetic resonance (NMR), Ultraviolet-visible (UV-Vis), and Electrospray ionization-mass spectrometry (ESI-MS). In the in vitro studies, Aca.B exhibited negligible toxicity and showed a dose-dependent nitric oxide inhibitory potential in Lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. In the in vivo studies, the oral administration of Aca.B to mice showed enhanced bioavailability and dose-dependent repression of the behavioral/cognitive impairment by regulating the cholinergic function, restoring the antioxidant status, attenuating the inflammatory cytokines/mediators and actively enriching neurotropic proteins in the hippocampal regions of the scopolamine-administered mice.

Keywords: Amnesia; Anti-AChE; Anti-inflammation; Antioxidant; Salicornia europaea L; Scopolamine; TrkB/CREB/BDNF.

MeSH terms

  • Amnesia / chemically induced*
  • Animals
  • Brain-Derived Neurotrophic Factor / metabolism
  • Cyclic AMP Response Element-Binding Protein / metabolism
  • Disease Models, Animal
  • Furans / pharmacology*
  • Glucosides / pharmacology*
  • Inflammation / metabolism*
  • Lignans / pharmacology*
  • Membrane Glycoproteins / metabolism
  • Mice
  • Oxidation-Reduction
  • Protein-Tyrosine Kinases / metabolism
  • Receptors, Cholinergic / metabolism*
  • Scopolamine / pharmacology

Substances

  • Bdnf protein, mouse
  • Brain-Derived Neurotrophic Factor
  • Creb1 protein, mouse
  • Cyclic AMP Response Element-Binding Protein
  • Furans
  • Glucosides
  • Lignans
  • Membrane Glycoproteins
  • Receptors, Cholinergic
  • acanthoside B
  • Scopolamine
  • Ntrk2 protein, mouse
  • Protein-Tyrosine Kinases