Intranasal administration of total bovine brain gangliosides (6 mg/kg) to rats protected the CA1 hippocampal neurons from the death caused by two-vessel occlusion model (with hypotension) of forebrain ischemia/reperfusion injury. The immunohistochemical reaction of specific antibodies to marker proteins of activated microglia (Iba1) and astrocytes (GFAP) in hippocampal slices revealed the neuroprotective effect of exogenous gangliosides which can be mostly explained by their ability to suppress neuroinflammation and gliosis. The expression of neurotrophic factor BDNF in the CA1 region of hippocampus did not differ in sham-operated rats and animals exposed to ischemia/reperfusion. However, the administration of gangliosides increased the BDNF expression in both control and ischemic groups. The intranasal route of administration allows using lower concentrations of gangliosides preventing the death of hippocampal neurons.

Original languageEnglish
Pages (from-to)736-742
Number of pages7
JournalBulletin of Experimental Biology and Medicine
Volume176
Issue number6
DOIs
StatePublished - 1 Apr 2024

    Research areas

  • Animals, Reperfusion Injury/pathology, Gangliosides/pharmacology, Rats, Administration, Intranasal, Male, CA1 Region, Hippocampal/drug effects, Brain-Derived Neurotrophic Factor/metabolism, Neurons/drug effects, Neuroprotective Agents/pharmacology, Rats, Wistar, Glial Fibrillary Acidic Protein/metabolism, Calcium-Binding Proteins/metabolism, Microfilament Proteins/metabolism, Brain Ischemia/drug therapy, Prosencephalon/drug effects, Astrocytes/drug effects, Microglia/drug effects, Cell Survival/drug effects, Disease Models, Animal, neuroinflammation, BDNF, gangliosides, ischemia, intranasal administration

ID: 124004569