Mito-Tempo prevents nicotine-induced exacerbation of ischemic brain damage

Nicotine may contribute to the pathogenesis of cerebrovascular disease via the generation of reactive oxygen species (ROS). Overproduction of ROS leads to brain damage by intensifying post-ischemic inflammation. Our goal was to determine the effect of Mito-Tempo, a mitochondria-targeted antioxidant, on ischemic brain damage and post-ischemic inflammation during chronic exposure to nicotine. Male Sprague-Dawley rats were divided into four groups: control, nicotine, Mito-Tempo-treated control, and Mito-Tempo-treated nicotine. Nicotine (2 mg/kg/day) was administered via an osmotic minipump for 4 weeks. Mito-Tempo (0.7 mg/kg/day IP) was given for 7 days prior to cerebral ischemia. Transient focal cerebral ischemia was induced by occlusion of the middle cerebral artery for 2 hours. Brain damage and inflammation were evaluated after 24 hours of reperfusion by measuring infarct volume, expression of adhesion molecules, activity of matrix metalloproteinase, brain edema, microglial activation and neutrophil infilt...