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先天性肌营养不良症 1D 模型中低强度训练对大脑和肌肉的影响。

Effects of low-intensity training on the brain and muscle in the congenital muscular dystrophy 1D model.

机构信息

Research Group in Neurodevelopment of Childhood and Adolescence, Laboratory of Experimental Neuroscience, Postgraduate Program in Health Sciences, University of South Santa Catarina (UNISUL), Avenida Pedra Branca, 25, Pedra Branca Palhoça, SC, 88137-270, Brazil.

Translational Psychiatry Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC), Criciúma, SC, Brazil.

出版信息

Neurol Sci. 2022 Jul;43(7):4493-4502. doi: 10.1007/s10072-022-05928-w. Epub 2022 Feb 19.

DOI:10.1007/s10072-022-05928-w
PMID:35182274
Abstract

INTRODUCTION

Congenital Muscular Dystrophy type 1D (MDC1D) is characterized by a hypoglycosylation of α-dystroglycan protein (α-DG), and this may be strongly implicated in increased skeletal muscle tissue degeneration and abnormal brain development, leading to cognitive impairment. However, the pathophysiology of brain involvement is still unclear. Low-intensity exercise training (LIET) is known to contribute to decreased muscle degeneration in animal models of other forms of progressive muscular dystrophies.

AIM

The objective of this study was to analyze the effects of LIET on cognitive involvement and oxidative stress in brain tissue and gastrocnemius muscle.

METHODS

Male homozygous (Large), heterozygous (Large), and wild-type mice were used. To complete 28 days of life, they were subjected to a low-intensity exercise training (LIET) for 8 weeks. After the last day of training, 24 h were expected when the animals were submitted to inhibitory avoidance and open-field test. The striatum, prefrontal cortex, hippocampus, cortex, and gastrocnemius were collected for evaluation of protein carbonylation, lipid peroxidation, and catalase and superoxide dismutase activity.

RESULTS

LIET was observed to reverse the alteration in aversive and habituation memory. Increased protein carbonylation in the striatum, prefrontal cortex, and hippocampus and lipid peroxidation in the prefrontal cortex and hippocampus were also reversed by LIET. In the evaluation of the antioxidant activity, LIET increased catalase activity in the hippocampus and cortex. In the gastrocnemius, LIET decreased the protein carbonylation and lipid peroxidation and increased catalase and superoxide dismutase activity.

CONCLUSION

In conclusion, it can be inferred that LIET for 8 weeks was able to reverse the cognitive damage and oxidative stress in brain tissue and gastrocnemius muscle in MDC1D animals.

摘要

引言

先天性肌营养不良症 1D 型(MDC1D)的特征是α- dystroglycan 蛋白(α-DG)的低糖化,这可能与骨骼肌组织退化和异常脑发育导致认知障碍密切相关。然而,脑受累的病理生理学仍不清楚。低强度运动训练(LIET)已知可减少其他形式进行性肌营养不良动物模型中的肌肉退化。

目的

本研究旨在分析 LIET 对大脑组织和腓肠肌认知障碍和氧化应激的影响。

方法

使用雄性纯合子(Large)、杂合子(Large)和野生型小鼠。为了完成 28 天的生命,它们接受了 8 周的低强度运动训练(LIET)。在训练的最后一天之后,预计动物将在 24 小时内进行抑制回避和旷场测试。采集纹状体、前额叶皮层、海马体、皮质和腓肠肌,以评估蛋白羰基化、脂质过氧化以及过氧化氢酶和超氧化物歧化酶的活性。

结果

LIET 可逆转厌恶和习惯记忆的改变。LIET 还逆转了纹状体、前额叶皮层和海马体中蛋白羰基化的增加以及前额叶皮层和海马体中脂质过氧化的增加。在抗氧化活性评价中,LIET 增加了海马体和皮质中的过氧化氢酶活性。在腓肠肌中,LIET 降低了蛋白羰基化和脂质过氧化,并增加了过氧化氢酶和超氧化物歧化酶的活性。

结论

总之,可以推断出 8 周的 LIET 能够逆转 MDC1D 动物的大脑组织和腓肠肌的认知损伤和氧化应激。

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