Earlier studies have demonstrated that exercise training can result in the diminishing of ischemic stroke-induced damages as well as BDNF misregulation. However, the underlying mechanisms of BDNF changes in response to ischemic stroke and exercise are still not entirely understood. Therefore, the aim of the current study was to determine whether high-intensity interval training (HIIT) in hippocampus of rat model of ischemic stroke intercedes PPARγ coactivator 1α (PGC1α)-pathway factors and BDNF regulation following induction of ischemic stroke. For this purpose, in this study, induction of middle cerebral artery occlusion (MCAO) was accomplished following the completion of HIIT. To define the molecular mechanisms that might be responsible for HIIT-associated improvements subsequent to cerebral ischemia, we likewise evaluated PGC-1α-pathway factors that may be essential for BDNF upregulation after MCAO via immunofluorescence tracking and ELISA immunoassay. Taking our findings together, three weeks of antecedent-HIIT resulted in more expression and delivery of BDNF in brain and plasma following MCAO through PGC-1α-pathway (p < 0.05). The present investigation also found a close relationship between expressed PGC-1α-pathway factors in brain and their concentrations in plasma (p < 0.05). In conclusion, findings of the current study exhibited that induction of cerebral ischemia as well as HIIT intervention both were associated with expression of PGC-1α-pathway factors in brain and their deliverance to blood. Consequently, these alterations may be considered as a protective factor against post-stroke neurological and functional disorders in the stroke model.
Keywords: Brain-derived neurotrophic factor; Cerebral ischemia; Exercise training; FNDC5.
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