Neuroprotective effects of chloroquine on neurological scores, blood-brain barrier permeability, and brain edema after traumatic brain injury in male rats
Autor: | Maryam Karimi, Somayeh Nazari, Faramarz Shirani, Vahid Alivirdiloo, Ali Siahposht-Khachaki, Sepehr Edalatkhah, Rama Khanian |
---|---|
Jazyk: | English<br />Korean |
Rok vydání: | 2023 |
Předmět: | |
Zdroj: | Journal of Neurocritical Care, Vol 16, Iss 1, Pp 18-27 (2023) |
Druh dokumentu: | article |
ISSN: | 2005-0348 2508-1349 |
DOI: | 10.18700/jnc.220052 |
Popis: | Background Traumatic brain injury (TBI) is one of the 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 |
Databáze: | Directory of Open Access Journals |
Externí odkaz: |