Suppr超能文献

跑步机训练可改善脑缺血性中风大鼠的神经功能缺损并抑制神经元凋亡。

Treadmill training improves neurological deficits and suppresses neuronal apoptosis in cerebral ischemic stroke rats.

作者信息

Cao Li-Mei, Dong Zhi-Qiang, Li Qiang, Chen Xu

机构信息

Department of Neurology, Shanghai No. 8 People's Hospital, Shanghai, China.

出版信息

Neural Regen Res. 2019 Aug;14(8):1387-1393. doi: 10.4103/1673-5374.253523.

Abstract

Rehabilitation training is believed to be beneficial to patients with stroke, but its molecular mechanism is still unclear. Rat models of cerebral ischemic stroke were established by middle cerebral artery occlusion/reperfusion, and then received treadmill training of different intensities, twice a day for 30 minutes for 1 week. Low-intensity training was conducted at 5 m/min, with a 10-minute running, 10-minute rest, and 10-minute running cycle. In the moderate-intensity training, the intensity gradually increased from 5 m/min to 10 m/min in 5 minutes, with the same rest cycle as above. In high-intensity training, the intensity gradually increased from 5 m/min to 25 m/min in 5 minutes, with the same rest cycle as above. The Bederson scale was used to evaluate the improvement of motor function. Infarct volume was detected using 2,3,5-triphenyltetrazolium chloride staining. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining was applied to detect the apoptosis of nerve cells in brain tissue. Western blot assay was employed to analyze the activation of cyclic adenosine monophosphate (cAMP)/protein kinase A and Akt/glycogen synthase kinase-3β signaling pathways in rat brain tissue. All training intensities reduced the neurological deficit score, infarct volume, and apoptosis in nerve cells in brain tissue of stroke rats. Training intensities activated the cAMP/protein kinase A and Akt/glycogen synthase kinase-3 beta signaling pathways. This activation was more obvious with higher training intensities. These changes were reversed by intracerebroventricular injection of protein kinase A inhibitor Rp-cAMP. Our findings indicate that the neuroprotective effect of rehabilitation training is achieved via activation of the cAMP/protein kinase A and Akt/glycogen synthase kinase-3 beta signaling pathways. This study was approved by the Ethics Committee of Animal Experimentation in Shanghai No. 8 People's Hospital, China.

摘要

康复训练被认为对中风患者有益,但其分子机制仍不清楚。通过大脑中动脉闭塞/再灌注建立大鼠脑缺血性中风模型,然后接受不同强度的跑步机训练,每天两次,每次30分钟,持续1周。低强度训练以5米/分钟的速度进行,跑步10分钟、休息10分钟、再跑步10分钟为一个循环。中等强度训练时,强度在5分钟内从5米/分钟逐渐增加到10米/分钟,休息循环与上述相同。高强度训练时,强度在5分钟内从5米/分钟逐渐增加到25米/分钟,休息循环与上述相同。使用贝德森量表评估运动功能的改善情况。采用2,3,5-三苯基氯化四氮唑染色检测梗死体积。应用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记染色检测脑组织中神经细胞的凋亡。采用蛋白质免疫印迹法分析大鼠脑组织中环磷酸腺苷(cAMP)/蛋白激酶A和Akt/糖原合酶激酶-3β信号通路的激活情况。所有训练强度均降低了中风大鼠脑组织中的神经功能缺损评分、梗死体积以及神经细胞凋亡。训练强度激活了cAMP/蛋白激酶A和Akt/糖原合酶激酶-3β信号通路。训练强度越高,这种激活越明显。脑室内注射蛋白激酶A抑制剂Rp-cAMP可逆转这些变化。我们的研究结果表明,康复训练的神经保护作用是通过激活cAMP/蛋白激酶A和Akt/糖原合酶激酶-3β信号通路实现的。本研究经中国上海市第八人民医院动物实验伦理委员会批准。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d39e/6524516/405f0fe4b5b9/NRR-14-1387-g002.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验