Treadmill training attenuates pyroptosis in rats with cerebral ischemia/reperfusion injury

OBJECTIVE(S): Few studies have investigated the mechanism by which exercise training promotes neural repair during rehabilitation after stroke. In this study, we evaluated the neuroprotective effects of exercise training and pyroptosis-associated factors in the penumbra and elucidated the possible mechanisms. MATERIALS AND METHODS: Neurological deficits, body weight, and the infarct size were evaluated, and haematoxylin-eosin (HE) staining was performed. Western blotting and immunofluorescence staining were used to assess NOD-like receptor family pyrin domain-containing 3 (NLRP3) and caspase-1 levels. Interleukin-1β (IL-1β) and interleukin-18 (IL-18) levels were assessed by enzyme-linked immunosorbent assay (ELISA). B-cell lymphoma 2 (bcl-2) and bax protein levels were measured by Western blotting, and terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) staining was used to evaluate apoptotic cells. RESULTS: Exercise training decreased neurological deficits and the infarct size in MCAO rats Moreover, NLRP3 inflammasome-associated protein levels in the peri-infarct cortex were decreased by exercise training. Exercise training decreased the serum concentrations of IL1β and IL18, upregulated bcl-2, downregulated bax, and reduced the TUNEL index. CONCLUSION: Exercise training suppresses NLRP3 inflammasome activity and inhibits pyroptosis to protect against cerebral ischaemic injury. Exercise training can also suppress apoptosis, which may be the target of exercise-induced neuroprotection, thereby reducing brain injury.