Chronic cerebral hypoperfusion (CCH) is an important clinical condition characterized by a prolonged reduction in cerebral blood flow that contributes to several neurodegenerative diseases, including vascular dementia and Alzheimer's disease. A number of rodent models of CCH have been developed that mimic the human pathological conditions of reduced cerebral perfusion. These models have been instrumental in elucidating the molecular and cellular mechanisms involved in CCH-induced brain damage. Oxidative stress is induced by perturbations in cellular pathways caused by CCH, including mitochondrial dysfunction, ion pump dysfunction, and adenosine triphosphate (ATP) depletion. The deleterious stress leads to the accumulation of reactive oxygen species (ROS) and exacerbates damage to neuronal structures, significantly impairing cognitive function. Among the various therapeutic strategies being evaluated, edaravone, a potent antioxidant, is emerging as a promising drug due to its neuroprotective properties against oxidative stress. Initially approved for use in ischemic stroke, research using rodent CCH models has shown that edaravone has significant efficacy in scavenging free radicals and ameliorating oxidative stress-induced neuronal damage under CCH conditions. This mini-review summarizes the current literature on the rodent models of CCH and then discusses the therapeutic potential of edaravone to reduce neuronal and vascular damage caused by CCH-induced oxidative stress.