Browsing by Author "Feifei Pei"
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Item Mitochondrial Proteins Unveil the Mechanism by Which Physical Exercise Ameliorates Memory, Learning and Motor Activity in Hypoxic Ischemic Encephalopathy Rat Model(MDPI, 2022-04-11) Fred Gendi; Feifei Pei; Yuan Wang; Haoye Li; Jia Fu; Cheng ChangBackground: 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.Item Treadmill Exercise Improves Brain Energy Metabolism, Motor, and Cognitive Functions in Hypoxic Ischemic Encephalopathy Mice Model(Research Square, 2022-08-24) Feifei Pei; Fred Gendi; Yuan Wang; Haoyue Li; Shijia Du; Susu Cui; Jia Fu; Cheng ChangMore evidence shows that the brain energy demands are enormous. This study aimed to examine the metabolism changes in the brain of hypoxic ischemic encephalopathy (HIE) mice model and to evaluate how treadmill exercise enhances brain metabolism. We used unilateral carotid common artery ligation mice model to simulate the clinical HIE patients. Several behavior tests were used to evaluate the motor and cognitive function impairment, western blot and immunofluorescence were used to assess the metabolism related protein changes in the different groups. Meanwhile, the HIE mice models were randomly divided into exercise training group (HIE-T) which were subjected to four weeks of treadmill exercise training and non-exercise training group (HIE-NT). The results revealed that there was decreased expression of glucose transporters GLUTs in HIE and an enhanced expression of monocarboxylate transporters MCTs, which is an important part of energy metabolism adaptation. After the period of treadmill exercise training, the expression of GLUT1 as well as MCT1 increased in the motor cortex of HIE mice model. Moreover, the mitochondrial cristae and edges were clear and intact under Transmission electron microscope compared with HIE-NT group. This suggests that increased brain energy attributed to treadmill exercise training shows promising therapeutic potential for HIE.