TL-2 attenuates β-amyloid induced neuronal apoptosis through the AKT/GSK-3β/β-catenin pathway

Int J Neuropsychopharmacol. 2014 Sep;17(9):1511-9. doi: 10.1017/S1461145714000315. Epub 2014 Mar 19.

Abstract

β-amyloid (Aβ)-mediated neuronal apoptosis contributes to the progression of Alzheimer's disease (AD), although the exact mechanism remains unclear. This study aimed to investigate whether Dalesconol B (TL-2), a potent immunosuppressive agent with an unusual carbon skeleton, could inhibit Aβ-induced apoptosis in vitro and in vivo and to explore the underlying mechanisms. Aβ(1-42) was injected to bilateral hippocampus of mice to make the AD models in vivo. TL-2 was able to cross the blood-brain barrier and attenuate memory deficits in the AD mice. TL-2 also inhibited Aβ(1-42)-induced neuronal apoptosis in vitro and in vivo. In addition, TL-2 could activate the AKT/GSK-3β pathway, and inhibition of AKT and activation of GSK-3β partially eliminated the neuroprotective effects of TL-2. Furthermore, TL-2 induced the nuclear translocation of β-catenin and enhanced its transcriptional activity through the AKT/GSK-3β pathway to promote neuronal survival. These results suggest that TL-2 might be a potential drug for AD treatment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease* / chemically induced
  • Alzheimer Disease* / complications
  • Alzheimer Disease* / drug therapy
  • Alzheimer Disease* / pathology
  • Amyloid beta-Peptides / toxicity
  • Animals
  • Apoptosis / drug effects*
  • Caspase 3 / metabolism
  • Caspase 9 / metabolism
  • Cells, Cultured
  • Cerebral Cortex / cytology
  • Cerebral Cortex / pathology
  • Chromones / pharmacology
  • Disease Models, Animal
  • Enzyme Inhibitors / pharmacology
  • Glycogen Synthase Kinase 3 / metabolism
  • Glycogen Synthase Kinase 3 beta
  • Humans
  • Maze Learning / drug effects
  • Memory Disorders / chemically induced
  • Memory Disorders / drug therapy
  • Mice
  • Morpholines / pharmacology
  • Neurons / drug effects*
  • Neuroprotective Agents / therapeutic use*
  • Oncogene Protein v-akt / metabolism
  • Peptide Fragments / toxicity
  • Polycyclic Aromatic Hydrocarbons / therapeutic use*
  • Signal Transduction / drug effects*
  • beta Catenin / metabolism

Substances

  • Amyloid beta-Peptides
  • Chromones
  • Enzyme Inhibitors
  • Morpholines
  • Neuroprotective Agents
  • Peptide Fragments
  • Polycyclic Aromatic Hydrocarbons
  • amyloid beta-protein (1-42)
  • beta Catenin
  • dalesconol B
  • 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
  • GSK3B protein, human
  • Glycogen Synthase Kinase 3 beta
  • Gsk3b protein, mouse
  • Oncogene Protein v-akt
  • Glycogen Synthase Kinase 3
  • Caspase 3
  • Caspase 9