线粒体蛋白揭示了体育锻炼改善低氧缺血性脑病大鼠模型记忆、学习和运动能力的机制。

BACKGROUND

Physical exercise has been shown to improve cognitive and motor functions, promoting neurogenesis and demonstrating therapeutic benefits in neurodegenerative disorders. Nonetheless, it is crucial to investigate the cellular and molecular mechanisms by which this occurs. The study aimed to investigate and evaluate the effect of swimming exercise on the changes of mitochondrial proteins in the brains of rats with hypoxic ischemic encephalopathy (HIE).

METHODS

the vertical pole and Morris water maze tests were used to assess the animals' motor and cognitive functions, and western blot and immunofluorescence of brain tissue were used to assess the biomarkers of mitochondrial apoptosis and cristae stability in response to exercise training. Four groups of rats were used: (1) sham sedentary group (SHAM, NT), (2) sham exercise training group (SHAM, T) (3) hypoxic ischemic encephalopathy sedentary group (HIE, NT), and (4) hypoxic ischemic encephalopathy exercise training group (HIE, T).

RESULTS

animals with HIE showed motor and cognitive deficits, as well as increased apoptotic protein expression. Exercise, on the other hand, improved motor and cognitive functions while also suppressing the expression of apoptotic proteins.

CONCLUSIONS

By stabilizing the mitochondrial cristae and suppressing the apoptotic cascade, physical exercise provided neuroprotection in hypoxic ischemia-induced brain injury.

背景

体育锻炼已被证明可以改善认知和运动功能，促进神经发生，并在神经退行性疾病中显示出治疗益处。然而，研究其发生的细胞和分子机制至关重要。本研究旨在探讨和评估游泳运动对缺氧缺血性脑病（HIE）大鼠大脑中线粒体蛋白变化的影响。

方法

采用垂直杆和 Morris 水迷宫测试评估动物的运动和认知功能，采用脑组织 Western blot 和免疫荧光检测评估线粒体凋亡和嵴稳定性的生物标志物对运动训练的反应。使用四组大鼠：（1）假手术安静组（SHAM，NT），（2）假手术运动训练组（SHAM，T），（3）缺氧缺血性脑病安静组（HIE，NT），和（4）缺氧缺血性脑病运动训练组（HIE，T）。