Objective:

Evaluating inflammatory mediators in transient middle cerebral artery occlusion (tMCAO)

Background:

Strokes are one of the leading causes of death- with ischemic strokes being the most common. Typically, this process occurs by which a thrombus or embolus occludes a major vessel within the brain leading to reduced blood flow (ischemia) precipitating damage to brain tissue. Large vessel occlusion is a critical event, in which a rapid response is required to ensure the survival of brain tissue. In a previous study from our lab, human blood samples were collected from pre-ictus and post-ictus from large vessel occlusion samples. This study found increases in interferon gamma in the post-ictus compared to the pre-ictus and intraarterial artery (distal control). There was no significant increase in T-cells. IFN-gamma is involved in the production of various inflammatory mediators, however, in the context of the stroke, it is not known where the IFN-gamma production is sourced from early in the stroke cascade. This study aims to recapture the evidence found in the human study within a mice model to further elucidate the role of interferon gamma following a transient vessel occlusion. 

Design/Methods:

This study uses oxygen-glucose deprivation in vitro methods and in vivo experiments to evaluate sources of inflammation in the pre-occlusion and post-occlusion blood samples following transient middle cerebral artery occlusion (tMCAO) in mice. 

Results:

An increase in IFN-gamma was observed in the mice following transient middle cerebral artery occlusion (tMCAO) in the post-occlusion sample compared to pre-occlusion sample. 

Conclusions: