Ginsenoside Rh2 reverses sleep deprivation-induced cognitive deficit in mice

Behav Brain Res. 2018 Sep 3:349:109-115. doi: 10.1016/j.bbr.2018.03.005. Epub 2018 Mar 12.

Abstract

Sleep deprivation (SD) negatively caused cognitive deficit, which was associated with oxidative stress induced damage. Ginsenoside Rh2 had the ability to protect against damage caused by reactive oxygen species in vitro, showing antioxidant property. Therefore, it was hypothesized that Ginsenoside Rh2 could prevent SD-induced cognitive deficit via its antioxidant properties. In this study, the effect of Ginsenoside Rh2 on memory impairment induced by sleep deprivation was investigated. The mice were sleep deprived continuously for 14 days using our self-made Sleep Interruption Apparatus (SIA). Ginsenoside Rh2 was administered intraperitoneally at two doses (20 and 40 μmol/kg) for 20 days. Thereafter, behavioral studies were conducted to test the learning and memory ability using object location recognition (OLR) experiment and passive avoidance (PA) test. Additionally, the oxidative stress parameters in the serum and the brain tissues (cortex and hippocampus) were assessed, including the superoxide dismutase (SOD) enzyme activity, the total antioxidant reactivity (TAR), the malondialdehyde (MDA) level, the glutathione (GSH) level, and the lipid peroxidation (LPO) content. The results revealed that SD impaired both spatial and non-spatial memory (P < 0.05). Treatment with Ginsenoside Rh2 at both doses prevented memory impairment induced by SD. Moreover, Ginsenoside Rh2 normalized the reduction of SOD and TAR activities in the serum (P < 0.01) and the decrease of GSH content in both the cortex and hippocampus (P < 0.05) induced by SD. Furthermore, Ginsenoside Rh2 significantly decreased the MDA level in the serum (P < 0.05) and the LPO content in both the cortex and hippocampus (P < 0.05) compared to SD group. In conclusion, sleep deprivation impaired both spatial and non-spatial memory and Ginsenoside Rh2 reversed this impairment, probably by preventing the oxidative stress damage in the body, including the serum and brain during sleep deprivation.

Keywords: Antioxidant; Ginsenoside Rh2; Learning and memory; Sleep deprivation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / pharmacology*
  • Avoidance Learning / drug effects
  • Avoidance Learning / physiology
  • Brain / drug effects
  • Brain / metabolism
  • Cognitive Dysfunction / drug therapy*
  • Cognitive Dysfunction / etiology*
  • Cognitive Dysfunction / metabolism
  • Dose-Response Relationship, Drug
  • Ginsenosides / pharmacology*
  • Male
  • Memory Disorders / drug therapy
  • Memory Disorders / etiology
  • Memory Disorders / metabolism
  • Mice, Inbred ICR
  • Motor Activity / drug effects
  • Motor Activity / physiology
  • Nootropic Agents / pharmacology*
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology
  • Random Allocation
  • Recognition, Psychology / drug effects
  • Recognition, Psychology / physiology
  • Sleep Deprivation / complications*
  • Sleep Deprivation / drug therapy
  • Sleep Deprivation / metabolism
  • Spatial Memory / drug effects
  • Spatial Memory / physiology

Substances

  • Antioxidants
  • Ginsenosides
  • Nootropic Agents
  • ginsenoside Rh2