Forced, not voluntary, exercise effectively induces neuroprotection in stroke.

摘要: Previous treadmill exercise studies showing neuroprotective effects have raised questions as to whether or the stress related it may be key etiologic factors. In this study, we examined different regimens (forced and voluntary exercise) compared them with effect of stress-only on stroke protection. Adult male Sprague-Dawley rats (n = 65) were randomly assigned treatment groups for 3 weeks. These included control, exercise, running wheel restraint, electric shock. Levels hormone, corticosterone, measured in using ELISA. Animals from each group then subjected induced by a 2-h middle cerebral artery (MCA) occlusion followed 48-h reperfusion. Infarct volume was determined group, while changes gene expression stress-induced heat shock proteins (Hsp) 27 70 real-time PCR between groups. The level corticosterone significantly higher both (P < 0.05) groups, but not group. reduced 0.01) following exercised treadmill. However, amelioration damage duplicated even though distance longer than that forced (4,828 vs. 900 m). Furthermore, displayed increased infarct volume. Expression Hsp mRNA results suggest stressful component, rather either alone, is better able reduce This exercise-induced neuroprotection attributable up-regulation 70.