| Objective: Stroke is the leading cause of death and disability in adults in China.Disability after stroke seriously affects the quality of life of surviving patients.With the continuous development of research in the field of neurorehabilitation,rehabilitation treatment after stroke has gradually been accepted by people.How to improve the quality of rehabilitation and how to reduce the rate of disability through rehabilitation have become the focus of current attention.Early rehabilitation interventions have been recommended in many guidelines.Studies have shown that early rehabilitation interventions have a better neuroprotective effect and are superior to late interventions in the speed and degree of functional recovery,but the optimal time point for early rehabilitation interventions is not yet clear.The purpose of this study was to observe the effects of exercise intervention at different time points on the nerve function and nerve plasticity of rats after middle cerebral artery infarction.And by observing the changes in the expression of Syn and BDNF in rats intervened in exercise intervention at different time points to explore the molecular mechanism of early rehabilitation intervention on neural plasticity and the optimal time point for rehabilitation intervention.Method: 24 male Sprague-Dawley(SD)rats were divided into 4 groups according to the random number table method,namely sham operation group(SHAM group),sedentary group(SED group),exercise after one day group(1D group),exercise after one week group(1W group)was involved,with 6 animals in each group.The middle cerebral artery occlusion(MCAO)modeling operation was completed by the Longa thread embolization method.Rats in the sham-operated group underwent the same procedure without inserting the thread embolism.Three days before modeling,all rats were preconditioned with treadmill exercise intervention and behavioral scoring.After the pre-adaptation,modeling surgery was performed.After modeling,rats meeting the criteria were selected for exercise intervention.The rats in SHAM group and SED group were placed on a stationary treadmill for 30 min/d.The rats in 1D group started exercise intervention one day after the successful modeling,and the rats in 1W group started exercise intervention one week after the successful modeling.All of them were 12m/min,and the frequency was 30min/d.All rats successfully modeled for eight weeks until the end of the intervention.One week,four weeks,and eight weeks after the successful modeling of each group of rats,the neurological function changes were detected by the modified neurological deficit score(m NSS),and the infarct volume changes were detected by MRI T2 WI sequence,and the changes in anisotropic score ratio(FA)was detected by diffusion tensor imaging sequence(DTI).After the eight-week exercise intervention,the integrity of corticospinal tract was detected by diffusion tensor tractography(DTT)technique,and the changes of Brain Derived Neurotrophic Factor and Synaptophysin content were detected by Western blot(WB).Results: One week after the successful modeling,the m NSS score and infarct volume ratio of the 1D group became lower than before and were significantly better than those of the SED group and the 1W group(P <0.05);meanwhile,the r FA of the 1D group was significantly higher than the SED group(P <0.05).Four weeks after the successful modeling,the infarct volume ratio of the 1D group was significantly lower than the 1W group(P <0.05);at the same time,the m NSS score(P <0.001),infarct volume ratio(P <0.001),r FA of the 1D group(P <0.01)were better than the SED group,and the differences were significant;the m NSS score(P <0.01),infarct volume ratio(P <0.05),r FA(P <0.05)of the 1W group were significantly better than the SED group.Eight weeks after successful modeling,the m NSS score and r FA of the 1D group were significantly better than the 1W group(P <0.05);the m NSS score,infarct volume ratio,r FA of the 1D group were better than those of SED group,the difference all were statistically significant(P <0.001);m NSS score(P <0.01),infarct volume ratio(P <0.01),r FA(P <0.05)in the 1W group were all significantly better than those in the SED group.Conclusion: The mechanism of early exercise intervention to promote neural plasticity may be related to the increased expression of Syn and BNDF protein in brain tissue.Early exercise intervention promotes cerebral nerve plasticity and nerve regeneration through increased expression of BDNF and Syn protein,improves r FA,promotes recovery of cortical spinal tract,reduces infarct volume,and finally achieves the purpose of improving nerve function.The effect of exercise intervention started one day after the successful modeling was better than the exercise intervention started one week after the successful modeling. |
PDF Full Text Request