Neuroprotective effect of Guanosine prevents mitochondrial dysfunction via modulation of glutamate transport in an in vitro model of brain ischemia

Stroke is a major cause of death worldwide and ischemic stroke represents 70% of all strokes globally. The rupture of energy metabolism is the hallmark of ischemic stroke, where the supply of oxygen and glucose is decreased. Mitochondria are the major source of reactive oxygen species and regulate apoptosis, functions critically implicated in the pathogenesis of cerebral ischemia. The endogenous nucleoside guanosine is a neuroprotective agent against glutamatergic excitotoxicity. Glutamate uptake demands increased energy to maintain ionic homeostasis which is supplied by increasing glycolysis and lactate production, and also depends on mithocondrial function.