Patients who receive major surgery often develop postoperative cognitive dysfunction (POCD); however, there is a lack of effective management as the pathogenesis of this disorder has not been fully elucidated. The neuroprotective effects of edaravone have been characterized in both in vitro cultured cells and in experimental animal models. The present study aimed to determine the potential role of edaravone in surgery-induced cognitive decline in mice. Animals were assigned to three groups: Control group (n=32), where mice received local anesthesia; surgery group (n=32), where mice underwent abdominal surgery under anesthesia; and edaravone group (n=32), where mice received abdominal surgery and were administered with edaravone (3 mg/kg). Morris water maze and T-maze tests demonstrated that edaravone attenuated surgery-induced cognitive impairment. Nissl staining indicated that edaravone prevented neuronal loss in the hippocampus of mice that underwent surgery. Furthermore, treatment with edaravone mitigated the surgery-induced upregulation of glucose-regulated protein 78 and CCAAT-enhancer-binding homologous protein and reduced the number of terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling-positive nuclei in mice hippocampi. In conclusion, edaravone may prevent POCD-induced neuronal apoptosis through attenuating endoplasmic reticulum stress.
Keywords: apoptosis; cognition; edaravone; endoplasmic reticulum stress.