Caveolin is the principal
protein of caveolae and has been implicated in the pathogenesis of
cerebral ischemia. To investigate whether changed expression of
caveolins has a pivotal role in focal
cerebral ischemia, we induced
middle cerebral artery occlusion (MCAo)-reperfusion and examined expression of
caveolins, inflammatory activation markers, and mediators of autophagic cell death. We also treated MCAo rats with forced exercise to determine its effects on neurological outcome. Particularly, spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were used to compare the effects of
hypertension on focal
cerebral ischemia. All MCAo groups showed neurological deficiencies, motor dysfunction, and disruption of balancing ability; however, these pathological changes were more severe in SHR than WKY rats. Expression of
caveolins was decreased in MCAo brain tissue, whereas the levels of iNOS and
glial fibrillary acidic protein (GFAP) increased. Additionally, LC3-II and
beclin-1 levels were elevated in the MCAo groups. Forced exercise attenuated both molecular and behavioral changes in MCAo animals, but SHR rats showed delayed functional recovery and residual molecular changes when compared to WKY rats. These results suggest that forced exercise may be beneficial for promoting functional recovery following
cerebral ischemia through
caveolin-dependent mechanisms or interactions between
caveolins and these signaling molecules in ischemic brain regions.