Neuroprotective effects of chloroquine on neurological scores, blood-brain barrier permeability, and brain edema after traumatic brain injury in male rats

Background: Traumatic brain injury (TBI) is one of leading causes of death among young people worldwide. Chloroquine, an antimalarial drug, has been shown to easily cross the blood-brain barrier (BBB) and inhibit autophagy in a variety of disorders, including Alzheimer disease and brain ischemia. We investigated the effects of chloroquine on neuronal protection after induction of brain trauma in male rats.Methods: A total of 120 male Wistar rats were treated with chloroquine at doses of 1.5, 3, and 6 mg/kg intraperitoneally after induction of diffuse TBIs. The veterinary coma scale was used to assess short-term neurological deficits. BBB disruption was evaluated using the Evans Blue dye method 6-hour post-injury. Vestibulomotor function was evaluated using the beam walk and beam balance methods. Histopathological changes in the brain tissue in different groups were evaluated using light microscopy and hematoxylin-eosin staining. Brain water and cerebrospinal fluid (CSF) contents of matrix metalloproteinase 9 (MMP-9) were assessed using the wet/dry method and enzyme-linked immunosorbent assay, respectively.Results: The results showed that injecting chloroquine (3 and 6 mg/kg) 30 minutes after TBI significantly reduced brain edema and BBB disruption, and recovered neurological deficits post-TBI (P