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通过对雄性斯普拉格-道利大鼠进行不同强度和持续时间的耐力训练来实现缺血性中风康复。

Ischemic stroke rehabilitation through endurance training of varying intensity and duration in male Sprague-Dawley rats.

作者信息

Fasihiyan Moein, Nourshahi Maryam, Taheri Maryam, Asadi Yasmin, Pakravan Reza

机构信息

Department of Biological Sciences in Sport and Health, Faculty of Sport Science and Health, Shahid Beheshti University, Tehran, Iran.

Department of Kinesiology and Physical Education, McGill University, Montréal, Quebec, Canada.

出版信息

Iran J Basic Med Sci. 2025;28(10):1363-1371. doi: 10.22038/ijbms.2025.86115.18602.

DOI:10.22038/ijbms.2025.86115.18602
PMID:40896700
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12399065/
Abstract

OBJECTIVES

This research aimed to investigate the effect of 2 types of exercise on apoptosis, neurogenesis, and angiogenesis factors in the penumbra area of stroke during the rehabilitation period after stroke.

MATERIALS AND METHODS

A transient distal middle cerebral artery occlusion (td-MCAO) model was used to induce stroke and after that, the animals were randomly divided into three groups: stroke, stroke + continuous exercise with increasing duration (CTID), and stroke + exercise with increasing intensity (CTII). At 24 hr spost-stroke , MRA, neurological deficit, and behavioral tests were conducted, and also continuous exercises were conducted for five consecutive days, Finally, MRI and behavioral tests were performed, and 24 hr after that, tissue separation and blood sampling were performed to evaluate plasma irisin, Extracellular Signal-Regulated Kinases 1 and 2 (ERK1/2) / cAMP Response Element-Binding Protein (CREB) / 90 kDa Ribosomal S6 Kinase (P90RSK) pathway, Vascular Endothelial Growth Factor (VEGF) / Vascular Endothelial Growth Factor Receptor 2 (VEGF-R2), and Brain-Derived Neurotrophic Factor (BDNF) / Tropomyosin Receptor Kinase B (TrKB) levels. for statistical analysis, one-way and two-way ANOVA tests were used at the significance level of P<0.05.

RESULTS

Both training models reduced the volume of stroke and neurological defects compared to the stroke group (<0.05), while the amounts of irisin and CREB in the CTID group increased significantly compared to the CTII and stroke groups (<0.01). VEGFR2 values in training groups increased significantly compared to the stroke group (<0.05) but in the CTII group, VEGFR2 values increased significantly compared to the CTID group (<0.05).

CONCLUSION

The findings of the present study showed it seems that doing exercises with moderate intensities and gradually increasing the duration of exercise in the acute phase after stroke can be considered a suitable treatment in future research.

摘要

目的

本研究旨在探讨两种运动方式对脑卒中康复期梗死灶周围半暗带区域细胞凋亡、神经发生及血管生成因子的影响。

材料与方法

采用短暂性大脑中动脉远端闭塞(td-MCAO)模型诱导脑卒中,之后将动物随机分为三组:脑卒中组、脑卒中+持续运动且运动时长增加组(CTID)、脑卒中+运动强度增加组(CTII)。脑卒中后24小时,进行磁共振血管造影(MRA)、神经功能缺损及行为学测试,并连续进行五天的持续运动。最后,进行磁共振成像(MRI)及行为学测试,之后24小时,进行组织分离及采血,以评估血浆鸢尾素、细胞外信号调节激酶1和2(ERK1/2)/环磷酸腺苷反应元件结合蛋白(CREB)/90 kDa核糖体S6激酶(P90RSK)通路、血管内皮生长因子(VEGF)/血管内皮生长因子受体2(VEGF-R2)以及脑源性神经营养因子(BDNF)/原肌球蛋白受体激酶B(TrKB)水平。统计学分析采用单因素和双因素方差分析,显著性水平为P<0.05。

结果

与脑卒中组相比,两种训练模式均减小了脑梗死体积并改善了神经功能缺损(P<0.05),而CTID组的鸢尾素和CREB含量与CTII组及脑卒中组相比显著增加(P<0.01)。与脑卒中组相比,训练组的VEGFR2值显著增加(P<0.05),但在CTII组中,VEGFR2值与CTID组相比显著增加(P<0.05)。

结论

本研究结果表明,在脑卒中急性期进行中等强度且逐渐增加运动时长的运动,在未来研究中可被视为一种合适的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/777c/12399065/46297c225a35/IJBMS-28-1363-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/777c/12399065/aeb289a89df7/IJBMS-28-1363-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/777c/12399065/1c6259fff053/IJBMS-28-1363-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/777c/12399065/e3516abe8d0d/IJBMS-28-1363-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/777c/12399065/2b3a8bef5c01/IJBMS-28-1363-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/777c/12399065/46297c225a35/IJBMS-28-1363-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/777c/12399065/aeb289a89df7/IJBMS-28-1363-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/777c/12399065/1c6259fff053/IJBMS-28-1363-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/777c/12399065/e3516abe8d0d/IJBMS-28-1363-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/777c/12399065/2b3a8bef5c01/IJBMS-28-1363-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/777c/12399065/46297c225a35/IJBMS-28-1363-g005.jpg

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