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1.
Journal of Southern Medical University ; (12): 1543-1546, 2011.
Article in Chinese | WPRIM | ID: wpr-333868

ABSTRACT

<p><b>OBJECTIVE</b>To determine the effect of willed movement on the expression of glial fibrillary acidic protein (GFAP) and synaptophysin (SYP) in adult rats with cerebral ischemia-reperfusion, and explore the mechanism of willed movement in promoting nerve repair and regeneration.</p><p><b>METHODS</b>Adult rat models of cerebral ischemia-reperfusion injury were established by middle cerebral artery occlusion (MCAO) for 2 h followed by a 24-h reperfusion. The models were then divided randomly into 3 groups, namely the model group, environmental modification (EM) group, and willed movement (WM) group. In each group, neurological deficits were evaluated at 3, 7 and 15 days after reperfusion. Immunohistochemistry and immunofluorescence assay were employed to examine the expression of GFAP and SYP in the brain tissue near the ischemic foci.</p><p><b>RESULTS</b>The rats in WM group showed lessened neurological deficits at 15 days and lowered expression of GFAP and SYP at 7 and 15 days after reperfusion compared with the model and EM groups (P<0.05). No significant difference was found in the expression of GFAP or SYP between the model group and EM group at any time points.</p><p><b>CONCLUSION</b>Willed movement can promote the functional recovery of neurological deficits following cerebral ischemia-reperfusion probably in relation to enhanced GFAP and SYP expressions in the ischemic brain tissues.</p>


Subject(s)
Animals , Male , Rats , Brain Ischemia , Metabolism , Therapeutics , Disease Models, Animal , Exercise Therapy , Methods , Glial Fibrillary Acidic Protein , Metabolism , Rats, Sprague-Dawley , Reperfusion Injury , Metabolism , Therapeutics , Synaptophysin , Metabolism
2.
Journal of Southern Medical University ; (12): 1401-1404, 2011.
Article in Chinese | WPRIM | ID: wpr-235115

ABSTRACT

<p><b>OBJECTIVE</b>To observe the effect of willed movement therapy on the expression of neurotrophin 3 (NT-3) and growth associated protein 43 (GAP-43) in rats with cerebral ischemia-reperfusion (IR) and investigate the neuroprotective mechanism of willed movement therapy in nerve regeneration and repair.</p><p><b>METHODS</b>Cerebral IR model was established by middle cerebral artery occlusion (MCAO) in SD rats. The rats were randomly divided into MCAO group, environment modification group (EM group) and willed movement therapy group (WM group). The rats were evaluated for neurological deficits and decapitated on days 3, 7 and 15 after the reperfusion to examine the expressions of NT-3 and GAP-43 in the ischemic brain tissues by immunohistochemistry.</p><p><b>RESULTS</b>Compared with MCAO and EM groups, the rats in WM group showed significantly lowered grade of neurological deficits (P<0.05) at 15 days and significantly increased the expressions of NT-3 and GAP-43 (P<0.05) at 7 and 15 days after the reperfusion. No significant difference was found in the expression of NT-3 and GAP-43 between MCAO and EM groups (P>0.05). The expression of NT-3 was positively correlated to that of GAP-43 in the ischemic tissues.</p><p><b>CONCLUSIONS</b>Willed movement therapy increases the expression of NT-3 and GAP-43 in the ischemic brain area in rats with cerebral ischemia-reperfusion, which is probably related to nerve regeneration and repair.</p>


Subject(s)
Animals , Male , Rats , Brain Ischemia , Metabolism , Therapeutics , Exercise Therapy , Methods , GAP-43 Protein , Metabolism , Infarction, Middle Cerebral Artery , Metabolism , Therapeutics , Movement , Physiology , Nerve Regeneration , Neuronal Plasticity , Physiology , Neurotrophin 3 , Metabolism , Physical Exertion , Physiology , Random Allocation , Rats, Sprague-Dawley , Reperfusion Injury , Metabolism , Therapeutics
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