The activation of AMPK/PGC-1α/GLUT4 signaling pathway through early exercise improves mitochondrial function and mitigates ischemic brain damage.

Mitochondria play a crucial role in maintaining cellular energy supply and serve as a source of energy for repairing nerve damage following a stroke. Given that exercise has the potential to enhance energy metabolism, investigating the impact of exercise on mitochondrial function provides a plausible mechanism for stroke treatment. In our study, we established the middle cerebral artery occlusion (MCAO) model in Sprague-Dawley rats and implemented early exercise intervention.

Early exercise intervention promotes myelin repair in the brains of ischemic rats by inhibiting the MEK/ERK pathway.

Our previous studies have shown that early exercise intervention after stroke increases neural activity and synaptic plasticity and promotes the recovery of nerve fiber bundle integrity in the brain. However, the effect of exercise on the repair of myelin in the brain and the related mechanism are still unclear. In this study, we randomly divided the rats into three groups.

Tactile stimulation promotes the recovery of motor function in rats with cerebral ischaemia.

Objectives: Tactile stimulation (TS) can promote neurogenesis and motor function recovery in rats with hypoxic-ischaemic brain injury, but the underlying mechanism is not clear. This study aimed to assess the effects of TS on neurological function in rats after cerebral ischaemia and explore the underlying mechanism.

Methods: Adult SD rats were randomly divided into a sham operation (SHAM) group, middle cerebral artery occlusion with tactile stimulation (TS-MCAO) group and middle cerebral artery occlusion with sedentary intervention (SED-MCAO) group.

Intermittent hypoxia promotes the recovery of motor function in rats with cerebral ischemia by regulating mitochondrial function.

Hypoxia preconditioning is neuroprotective, but the therapeutic effects of intermittent hypoxia were not fully considered. The present study investigated the neuroprotective effect and mechanism of intermittent hypoxia on motor function after cerebral ischemia and explored alternative clinical treatment options. In total, 36 8-week-old male Sprague-Dawley rats were subjected to 60 min of transient middle cerebral artery occlusion (tMCAO) and then randomly divided into a sham-operated group (SHAM), tMCAO-sedentary group (SED), and tMCAO-intermittent hypoxia group (IH).

Exercise Intervention Promotes the Growth of Synapses and Regulates Neuroplasticity in Rats With Ischemic Stroke Through Exosomes.

Stroke is the leading cause of death and disability. Exercise produces neuroprotection by improving neuroplasticity. Exercise can induce exosome production.