Mangiferin ameliorates aluminium chloride-induced cognitive dysfunction via alleviation of hippocampal oxido-nitrosative stress, proinflammatory cytokines and acetylcholinesterase level

J Trace Elem Med Biol. 2015:31:107-12. doi: 10.1016/j.jtemb.2015.04.002. Epub 2015 Apr 22.

Abstract

Mangiferin is a phytochemical primarily present in the stem, leaves and bark of Mangifera indica. It offers neuroprotection mainly through inhibition of oxidative stress, and decreasing proinflammatory cytokines level in the brain. Aluminium has been reported to cause oxidative stress-associated damage in the brain. In the present investigation, protective effect of mangiferin against aluminium chloride (AlCl3)-induced neurotoxicity and cognitive impairment was studied in male Swiss albino mice. AlCl3 (100 mg/kg) was administered once daily through oral gavage for 42 days. Mangiferin (20 and 40 mg/kg, p.o.) was given to mice for last 21 days of the study. We found cognitive dysfunction in AlCl3-treated group, which was assessed by Morris water maze test, and novel object recognition test. AlCl3-treated group showed elevated level of oxidative stress markers, proinflammatory cytokines level and lowered hippocampal brain-derived neurotrophic factor (BDNF) content. Mangiferin (40 mg/kg) prevented the cognitive deficits, hippocampal BDNF depletion, and biochemical anomalies induced by AlCl3-treatment. In conclusion, our data demonstrated that mangiferin offers neuroprotection in AlCl3-induced neurotoxicity and it may be a potential therapeutic approach in the treatment of oxido-nitrosative stress and inflammation-associated neurotoxicity.

Keywords: Aluminium chloride; Cognitive dysfunction; Mangiferin; Neurotoxicity; Oxido-nitrosative stress.

MeSH terms

  • Acetylcholinesterase / metabolism
  • Aluminum Chloride
  • Aluminum Compounds / antagonists & inhibitors*
  • Aluminum Compounds / toxicity
  • Animals
  • Behavior, Animal / drug effects
  • Biomarkers / chemistry
  • Biomarkers / metabolism
  • Brain-Derived Neurotrophic Factor / agonists
  • Brain-Derived Neurotrophic Factor / antagonists & inhibitors
  • Brain-Derived Neurotrophic Factor / metabolism
  • Chlorides / antagonists & inhibitors*
  • Chlorides / toxicity
  • Cholinesterase Inhibitors / administration & dosage
  • Cholinesterase Inhibitors / therapeutic use*
  • Cytokines / antagonists & inhibitors
  • Cytokines / metabolism
  • Dose-Response Relationship, Drug
  • GPI-Linked Proteins / agonists
  • GPI-Linked Proteins / antagonists & inhibitors
  • GPI-Linked Proteins / metabolism
  • Hippocampus / drug effects*
  • Hippocampus / immunology
  • Hippocampus / metabolism
  • Lipid Peroxidation / drug effects
  • Male
  • Maze Learning / drug effects
  • Mice
  • Nerve Tissue Proteins / agonists
  • Nerve Tissue Proteins / antagonists & inhibitors
  • Nerve Tissue Proteins / metabolism
  • Neurons / drug effects
  • Neurons / immunology
  • Neurons / metabolism
  • Neuroprotective Agents / administration & dosage
  • Neuroprotective Agents / therapeutic use*
  • Neurotoxicity Syndromes / immunology
  • Neurotoxicity Syndromes / metabolism
  • Neurotoxicity Syndromes / prevention & control*
  • Oxidative Stress / drug effects*
  • Random Allocation
  • Water Pollutants, Chemical / antagonists & inhibitors
  • Water Pollutants, Chemical / toxicity
  • Xanthones / administration & dosage
  • Xanthones / therapeutic use*

Substances

  • Aluminum Compounds
  • Biomarkers
  • Brain-Derived Neurotrophic Factor
  • Chlorides
  • Cholinesterase Inhibitors
  • Cytokines
  • GPI-Linked Proteins
  • Nerve Tissue Proteins
  • Neuroprotective Agents
  • Water Pollutants, Chemical
  • Xanthones
  • mangiferin
  • Aluminum Chloride
  • Acetylcholinesterase
  • Ache protein, mouse