Neuroprotective Effects of Soy Isoflavones on Scopolamine-Induced Amnesia in Mice

Nutrients. 2018 Jun 30;10(7):853. doi: 10.3390/nu10070853.

Abstract

In the recent years, interest in soybean as a neuroprotective nutrient in the management of Alzheimer’s disease (AD) has increased and soy isoflavones (SI), as kinds of soybean phytochemicals, are thought to be biologically active components that confer this beneficial effect against neurodegenerative diseases. However, the neuroprotective effect of SI is not well understood. Therefore, the present study (30 days) was conducted to investigate the neuroprotective effects of soy isoflavones (SI) on scopolamine (SCOP)-induced memory impairments in Institute of Cancer Research (ICR) mice (aged 4 weeks) and to elucidate its underlying mechanisms of action. SI (40 mg/kg) administration improved the cognitive performance of SCOP-treated mice in an object location recognition task and the Morris water maze test. SI (40 mg/kg) administration significantly enhanced cholinergic system function and suppressed oxidative stress levels in the hippocampus of SCOP-treated mice. Furthermore, SI (40 mg/kg) treatment markedly upregulated the phosphorylation levels of extracellular signal-regulated kinase (ERK), cAMP response element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF) expression levels in the hippocampus. Taken together, these results demonstrated that soy isoflavones exerted a significant neuroprotective effect on cognitive dysfunctions induced by scopolamine, suggesting that soy isoflavones could be a good candidate for possible treatment of neurodegenerative diseases, such as Alzheimer’s disease (AD).

Keywords: ERK/CREB/BDNF pathway; cholinergic system function; learning and memory; oxidative stress; scopolamine; soy isoflavones.

MeSH terms

  • Acetylcholine / metabolism
  • Acetylcholinesterase / metabolism
  • Amnesia / chemically induced
  • Amnesia / metabolism
  • Amnesia / prevention & control*
  • Amnesia / psychology
  • Animals
  • Antioxidants / pharmacology
  • Behavior, Animal / drug effects*
  • Brain-Derived Neurotrophic Factor / metabolism
  • Choline O-Acetyltransferase / metabolism
  • Cholinergic Neurons / drug effects
  • Cholinergic Neurons / metabolism
  • Cognition / drug effects
  • Cyclic AMP Response Element-Binding Protein / metabolism
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • GPI-Linked Proteins / metabolism
  • Glycine max* / chemistry
  • Hippocampus / drug effects*
  • Hippocampus / metabolism
  • Hippocampus / physiopathology
  • Isoflavones / isolation & purification
  • Isoflavones / pharmacology*
  • Male
  • Maze Learning / drug effects
  • Memory / drug effects*
  • Mice, Inbred ICR
  • Neuroprotective Agents / isolation & purification
  • Neuroprotective Agents / pharmacology*
  • Oxidative Stress / drug effects
  • Phosphorylation
  • Scopolamine*
  • Time Factors

Substances

  • Antioxidants
  • Brain-Derived Neurotrophic Factor
  • Creb1 protein, mouse
  • Cyclic AMP Response Element-Binding Protein
  • GPI-Linked Proteins
  • Isoflavones
  • Neuroprotective Agents
  • Scopolamine
  • Choline O-Acetyltransferase
  • Extracellular Signal-Regulated MAP Kinases
  • Acetylcholinesterase
  • Ache protein, mouse
  • Acetylcholine