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Strength exercise suppresses STZ-induced spatial memory impairment and modulates BDNF/ERK-CAMKII/CREB signalling pathway in the hippocampus of mice.
CELL BIOCHEMISTRY AND FUNCTION ( IF 3.6 ) Pub Date : 2020-01-24 , DOI: 10.1002/cbf.3470
Franciele Martini 1 , Marlon Régis Leite 1 , Suzan Gonçalves Rosa 1 , Isabella Pregardier Klann 1 , Cristina Wayne Nogueira 1
Affiliation  

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that has generated scientific interest because of its prevalence in the population. Studies indicate that physical exercise promotes neuroplasticity and improves cognitive function in animal models and in human beings. The aim of the present study was to investigate the effects of strength exercise on the hippocampal protein contents and memory performance in mice subjected to a model of sporadic AD induced by streptozotocin (STZ). Swiss mice received two injections of STZ (3 mg/kg, intracerebroventricular). After 21 days, they began physical training using a ladde. Mice performed this protocol for 4 weeks. After the last exercise training session, mice performed the Morris Water Maze test. The samples of hippocampus were excised and used to determine protein contents of brain-derived neurotrophic factor (BDNF), extracellular signal-regulated kinase-Ca2+ (ERK), calmodulin-dependent protein kinase (CAMKII) and cAMP-response element-binding protein (CREB) signalling pathway. Strength exercise was effective against the decrease in the time spent and distance travelled in the target quadrant by STZ-injected mice. Strength exercise was also effective against the reduction of mature BDNF, tropomyosin receptor kinase B and neuronal nuclear antigen (NeuN) hippocampal protein levels in STZ mice. The decrease in the hippocampal ratio of pERK/ERK, pCAMKII/CAMKII and pCREB/CREB induced by STZ was reversed by strength exercise. Strength exercise decreased Bax/Bcl2 ratio in the hippocampus of STZ-injected mice. The present study demonstrates that strength exercise modulated the hippocampal BDNF/ERK-CAMKII/CREB signalling pathway and suppressed STZ-induced spatial memory impairment in mice.

中文翻译:

力量运动抑制小鼠海马中STZ诱导的空间记忆障碍并调节BDNF / ERK-CAMKII / CREB信号通路。

阿尔茨海默氏病(AD)是一种进行性神经退行性疾病,由于其在人群中的普遍性而引起了科学兴趣。研究表明,体育锻炼可促进动物模型和人类的神经可塑性并改善其认知功能。本研究的目的是研究在链脲佐菌素(STZ)诱导的散发性AD模型小鼠中,力量运动对海马蛋白含量和记忆性能的影响。瑞士小鼠接受了两次STZ注射(3 mg / kg,脑室内)。21天后,他们开始使用小伙子进行体育锻炼。小鼠执行该方案4周。在最后一次运动训练之后,小鼠进行了莫里斯水迷宫测试。切除海马样本并用于测定脑源性神经营养因子(BDNF),细胞外信号调节激酶Ca2 +(ERK),钙调蛋白依赖性蛋白激酶(CAMKII)和cAMP反应元件结合蛋白( CREB)信号通路。力量锻炼可有效减少注射STZ的小鼠在目标象限中花费的时间和移动的距离。力量运动还可以有效减少STZ小鼠中成熟BDNF,原肌球蛋白受体激酶B和神经元核抗原(NeuN)海马蛋白水平的降低。STZ诱导的海马pERK / ERK,pCAMKII / CAMKII和pCREB ​​/ CREB的海马比例的降低可通过力量运动逆转。力量运动可降低注射STZ的小鼠海马中的Bax / Bcl2比。
更新日期:2020-01-24
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