Fermented rice peptides attenuate scopolamine-induced memory impairment in mice by regulating neurotrophic signaling pathways in the hippocampus

Brain Res. 2019 Oct 1:1720:146322. doi: 10.1016/j.brainres.2019.146322. Epub 2019 Jul 3.

Abstract

This study investigated the preventive effects of fermented rice peptides (FRPs) against scopolamine-induced memory impairment in mice and their potential mechanisms. Mice were pretreated with FRPs (25 and 100 mg/kg body weight) via intraperitoneal injection for 7 days, followed by intraperitoneal injection of scopolamine. FRP pretreatment suppressed scopolamine-induced cognitive impairment in passive-avoidance test and significantly upregulated levels of brain-derived neurotrophic factor (BDNF) and induced the phosphorylation of cAMP response element binding (CREB) protein and extracellular signal-regulated kinase (ERK) in the hippocampus of scopolamine-treated mice. Additionally, scopolamine-treated mice showed significantly decreased acetylcholine levels and increased acetylcholine-esterase activity in the hippocampus as compared with controls; however, these changes were suppressed by FRP pretreatment. Among the fractions separated by size-exclusion chromatography, the non-glycosylated peptide fraction of FRP suppressed H2O2-induced neuronal damage in SK-N-SH cells via upregulated BDNF levels. Our findings demonstrated that FRP prevented memory impairment, and that the underlying mechanism might involve regulation of the ERK/CREB/BDNF signaling pathway. These results suggest FRP as a potential agent for the prevention of age-related cognitive decline and dementia.

Keywords: Acetylcholine; Brain-derived neurotrophic factor; Cognitive impairment; Fermented rice; Peptides.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholinesterase / metabolism
  • Animals
  • Brain-Derived Neurotrophic Factor / metabolism
  • Cognitive Dysfunction / metabolism
  • Cyclic AMP Response Element-Binding Protein / metabolism
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Fermented Foods
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Hydrogen Peroxide / metabolism
  • Memory / drug effects
  • Memory Disorders / chemically induced
  • Memory Disorders / drug therapy*
  • Memory Disorders / metabolism
  • Mice
  • Nerve Growth Factors
  • Oryza / metabolism
  • Peptides / pharmacology*
  • Phosphorylation
  • Scopolamine / metabolism
  • Signal Transduction / drug effects
  • Temporal Lobe / metabolism

Substances

  • Bdnf protein, mouse
  • Brain-Derived Neurotrophic Factor
  • Creb1 protein, mouse
  • Cyclic AMP Response Element-Binding Protein
  • Nerve Growth Factors
  • Peptides
  • Hydrogen Peroxide
  • Scopolamine
  • Extracellular Signal-Regulated MAP Kinases
  • Acetylcholinesterase