About me
Electronic cigarette exposure worsens stroke induced inflammation and cognitive deficits in female rats.
Location: East Ballroom
Mentor: Dr. Ami Raval
The innate immune response plays a crucial role in the pathogenesis of ischemic stroke, with the inflammasome acting as a key component. In a previous study, we observed heightened inflammasome activation in the brains of nicotine-exposed female rats following ischemia. As nicotine is the primary psychoactive agent in both conventional and electronic cigarettes (ECs), understanding the impact of EC exposure on the brain remains essential. In our recent publication, we demonstrated that EC exposure worsens ischemic brain injury in female rats. Building on these findings, the current study aims to evaluate the effect of EC exposure on post-ischemic inflammasome activation in male and female rat brains. Since microglia mediate key components of both innate and adaptive immune responses post-ischemia, we also examined how EC exposure and stroke influence microglial activation. Adult male and female Sprague-Dawley rats were exposed to EC vapor (5% nicotine, Juul pods) or air for 16 consecutive nights, followed by transient middle cerebral artery occlusion (tMCAO; 90 minutes) or sham surgery. Animals were then assigned to two cohorts. In the first cohort, brains were harvested 24 hours post-stroke/sham for western blot analysis of inflammasome proteins. Female rats showed elevated levels of caspase-1 and ASC in the ipsilateral cortex post-tMCAO. In a subsequent cohort, animals were sacrificed 21 days post-tMCAO for immunohistochemical analysis of microglial marker Iba-1. Quantification using the optical fractionator in StereoInvestigator revealed increased microglial activation in the cortex of EC-exposed females, potentially contributing to worsened infarction after stroke.
