Dendrobium officinale polysaccharides attenuate learning and memory disabilities via anti-oxidant and anti-inflammatory actions

Int J Biol Macromol. 2019 Apr 1:126:414-426. doi: 10.1016/j.ijbiomac.2018.12.230. Epub 2018 Dec 26.

Abstract

The aim of this study was to explore the therapeutic effect and underling mechanism of Dendrobium officinale polysaccharides (DOPS) on two well-established animal models of learning and memory disabilities. Model of estrogen deficiency caused learning and memory disability can be induced by ovariectomy in mice, and mice were injected subcutaneously with d-galactose, which can also cause cognitive decline. H&E staining and Nissl staining were employed to confirm the protective effect of DOPS on hippocampal neuron. Morris water maze test, biochemical analysis, immunohistochemistry and immunofluorescence assay were used to study the effect and underlying mechanism of DOPS on two different learning and memory impairment models. Administration of DOPS significantly improved learning and memory disability in both models. Further studies showed that DOPS could attenuate oxidative stress and reduce neuro-inflammation via up-regulating expressions of Nrf2/HO-1 pathway and inhibiting activation of astrocytes and microglia in ovariectomy- and d-galactose-induced cognitive decline. These findings suggest that DOPS have an appreciable therapeutic effect on learning and memory disabilities and its mechanism may be related to activate Nrf2/HO-1 pathway to reduce oxidative stress and neuro-inflammation.

Keywords: Dendrobium officinale; Learning and memory impairment; Neuro-inflammation; Oxidative stress; Polysaccharides.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Anti-Inflammatory Agents / therapeutic use
  • Antioxidants / pharmacology*
  • Antioxidants / therapeutic use
  • Calcium-Binding Proteins / metabolism
  • Dendrobium / chemistry*
  • Female
  • Galactose
  • Glial Fibrillary Acidic Protein / metabolism
  • Heme Oxygenase-1 / metabolism
  • Hippocampus / metabolism
  • Hippocampus / pathology
  • Interleukin-1beta / metabolism
  • Malondialdehyde / metabolism
  • Memory / drug effects*
  • Memory Disorders / chemically induced
  • Memory Disorders / drug therapy
  • Memory Disorders / pathology
  • Mice
  • Microfilament Proteins / metabolism
  • Models, Biological
  • NF-E2-Related Factor 2 / metabolism
  • Neurons / drug effects
  • Neurons / pathology
  • Neuroprotective Agents / pharmacology
  • Neuroprotective Agents / therapeutic use
  • Nissl Bodies / drug effects
  • Nissl Bodies / metabolism
  • Ovariectomy
  • Oxidation-Reduction
  • Polysaccharides / pharmacology*
  • Signal Transduction / drug effects
  • Superoxide Dismutase / blood
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Aif1 protein, mouse
  • Anti-Inflammatory Agents
  • Antioxidants
  • Calcium-Binding Proteins
  • Glial Fibrillary Acidic Protein
  • Interleukin-1beta
  • Microfilament Proteins
  • NF-E2-Related Factor 2
  • Neuroprotective Agents
  • Polysaccharides
  • Tumor Necrosis Factor-alpha
  • Malondialdehyde
  • Heme Oxygenase-1
  • Superoxide Dismutase
  • Galactose