Aims: Exercise training has a neuroprotective effect against ischaemic injury, but the underlying mechanism is not completely clear. This study explored the potential mechanisms underlying the protective effects of treadmill training and caveolin-1 regulation against mitochondrial dysfunction in cerebral ischaemic injury.
Main Methods: After middle cerebral artery occlusion (MCAO) surgery, rats were subjected to treadmill training and received daidzein injections and combined therapy. A series of analyses, including neurological function scoring; body weight measurement; Nissl, haematoxylin and eosin staining; cerebral infarction volume assessment; mitochondrial morphology examination; caveolin-1, cytoplasmic and mitochondrial cytochrome C (CytC), and translocase of outer membrane 20 (TOM20) expression analysis; apoptosis index analysis; and transmission electron microscopy were conducted.
Key Findings: Treadmill training increased caveolin-1 expression, reduced neurobehavioral scores and cerebral infarction volumes, improved tissue morphology, reduced neuronal loss, inhibited mitochondrial outer membrane permeabilization (MOMP) through the caveolin-1 pathway, prevented excessive Cyt-C release from mitochondria, and reduced the degrees of apoptosis and mitochondrial damage. In addition, treadmill training increased the expression of TOM20 through the caveolin-1 pathway and maintained import signal function, thereby protecting mitochondrial integrity.
Significance: Treadmill exercise protected mitochondrial integrity and inhibited the endogenous mitochondrial apoptosis pathway. The damage of cerebral ischaemia was alleviated in rats through enhancement of caveolin-1 by treadmill exercise.
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