Bupropion Showed Neuroprotective Impacts Against Cerebral Ischemia/Reperfusion Injury by Reducing Oxidative Stress and Inflammation.

Abstract

Background: Cerebral ischemia/reperfusion (I/R) injury is the most prevalent form of brain stroke, affecting many patients worldwide. It is believed that oxidative stress and inflammation play major roles in the damage that occurs after the initiation of the disease.

Objectives: Therefore, for the first time, the current study aimed to investigate the neuroprotective effects of bupropion against cerebral I/R damage in a rat model.

Methods: Forty male rats were divided into four groups: Control, cerebral I/R, and two diseased groups that received 60 and 100 mg/kg of bupropion. One day after induction of the disease, behavioral tests, including grid walking, novel object recognition, and modified neurological severity score (mNSS), were performed on the rats. The levels of inflammatory cytokines, including IL-1β, TNF-α, IL-6, and IL-10, were measured in the rats' brain homogenates. Additionally, the levels of MDA, catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), and NO₂ ^- were measured.

Results: Bupropion administration was associated with improved performance in the novel object recognition and grid walking behavioral tests, as well as in the neurological disorder scores, in cerebral I/R rats. Moreover, BCAAO-induced inflammation was reduced by the administration of this drug, evidenced by reduced levels of cytokines IL-1β, TNF-α, and IL-6 and upregulation of IL-10. Additionally, membrane lipid peroxidation was reduced in the cerebral I/R rats receiving 100 mg/kg bupropion, and the level of SOD activity was improved in these animals. Finally, the administration of bupropion prevented the increase in NO₂ ^- levels induced by BCAAO.

Conclusions: In conclusion, bupropion has neuroprotective effects against cerebral I/R damage by reducing inflammation and oxidative stress in the brain.