Gallic acid improves recognition memory and decreases oxidative-inflammatory damage in the rat hippocampus with metabolic syndrome

Synapse. 2020 Feb;75(2):e22186. doi: 10.1002/syn.22186. Epub 2020 Sep 1.


Metabolic syndrome (MS) results from excessive consumption of high-calorie foods and sedentary lifestyles. Clinically, insulin resistance, abdominal obesity, hyperglycemia, dyslipidemia, and hypertension are observed. MS has been considered a risk factor in the development of dementia. In the brain, a metabolically impaired environment generates oxidative stress and excessive production of pro-inflammatory cytokines that deteriorate the morphology and neuronal function in the hippocampus, leading to cognitive impairment. Therapeutic alternatives suggest that phenolic compounds can be part of the treatment for neuropathies and metabolic diseases. In recent years, the use of Gallic Acid (GA) has demonstrated antioxidant and anti-inflammatory effects that contribute to neuroprotection and memory improvement in animal models. However, the effect of GA on hippocampal neurodegeneration and memory impairment under MS conditions is still unclear. In this work, we administered GA (20 mg/kg) for 60 days to rats with MS. The results show that GA treatment improved zoometric and biochemical parameters, as well as the recognition memory, in animals with MS. Additionally, GA administration increased hippocampal dendritic spines and decreased oxidative stress and inflammation. Our results show that GA treatment improves metabolism: reducing the oxidative and inflammatory environment that facilitates the recovery of the neuronal morphology in the hippocampus of rats with MS. Consequently, the recognition of objects by these animals, suggesting that GA could be used therapeutically in metabolic disorders that cause dementia.

Keywords: Golgi-Cox stain; dendritic spines; interleukins; novel objects; polyphenols; reactive oxygen species.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Glucose / drug effects
  • Blood Glucose / metabolism
  • Catalase / drug effects
  • Catalase / metabolism
  • Dendrites / drug effects
  • Dendrites / pathology
  • Gallic Acid / pharmacology*
  • Hippocampus / drug effects*
  • Hippocampus / metabolism
  • Hippocampus / pathology
  • Inflammation / metabolism
  • Insulin / blood
  • Interleukin-1beta / drug effects
  • Interleukin-1beta / metabolism
  • Memory / drug effects
  • Metabolic Syndrome / metabolism*
  • Oxidative Stress / drug effects
  • Rats
  • Reactive Oxygen Species / metabolism
  • Recognition, Psychology / drug effects*
  • Superoxide Dismutase / drug effects
  • Superoxide Dismutase / metabolism
  • Tumor Necrosis Factor-alpha / drug effects
  • Tumor Necrosis Factor-alpha / metabolism


  • Blood Glucose
  • IL1B protein, rat
  • Insulin
  • Interleukin-1beta
  • Reactive Oxygen Species
  • Tumor Necrosis Factor-alpha
  • Gallic Acid
  • Catalase
  • Superoxide Dismutase