Mitochondrial Proteins Unveil the Mechanism by Which Physical Exercise Ameliorates Memory, Learning and Motor Activity in Hypoxic Ischemic Encephalopathy Rat Model.

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Title: Mitochondrial Proteins Unveil the Mechanism by Which Physical Exercise Ameliorates Memory, Learning and Motor Activity in Hypoxic Ischemic Encephalopathy Rat Model.
Authors: Gendi, Fred, Pei, Feifei, Wang, Yuan, Li, Haoye, Fu, Jia, Chang, Cheng
Source: International Journal of Molecular Sciences; Apr2022, Vol. 23 Issue 8, p4235-4235, 15p
Subject Terms: CEREBRAL anoxia-ischemia, MITOCHONDRIAL proteins, MOTOR learning, TREADMILL exercise, OXYGEN consumption, SCOPOLAMINE, ANIMAL disease models, ACTIVE learning
Abstract: 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. [ABSTRACT FROM AUTHOR]
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  Label: Title
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  Data: Mitochondrial Proteins Unveil the Mechanism by Which Physical Exercise Ameliorates Memory, Learning and Motor Activity in Hypoxic Ischemic Encephalopathy Rat Model.
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  Data: <searchLink fieldCode="AR" term="%22Gendi%2C+Fred%22">Gendi, Fred</searchLink><br /><searchLink fieldCode="AR" term="%22Pei%2C+Feifei%22">Pei, Feifei</searchLink><br /><searchLink fieldCode="AR" term="%22Wang%2C+Yuan%22">Wang, Yuan</searchLink><br /><searchLink fieldCode="AR" term="%22Li%2C+Haoye%22">Li, Haoye</searchLink><br /><searchLink fieldCode="AR" term="%22Fu%2C+Jia%22">Fu, Jia</searchLink><br /><searchLink fieldCode="AR" term="%22Chang%2C+Cheng%22">Chang, Cheng</searchLink>
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  Data: International Journal of Molecular Sciences; Apr2022, Vol. 23 Issue 8, p4235-4235, 15p
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  Data: <searchLink fieldCode="DE" term="%22CEREBRAL+anoxia-ischemia%22">CEREBRAL anoxia-ischemia</searchLink><br /><searchLink fieldCode="DE" term="%22MITOCHONDRIAL+proteins%22">MITOCHONDRIAL proteins</searchLink><br /><searchLink fieldCode="DE" term="%22MOTOR+learning%22">MOTOR learning</searchLink><br /><searchLink fieldCode="DE" term="%22TREADMILL+exercise%22">TREADMILL exercise</searchLink><br /><searchLink fieldCode="DE" term="%22OXYGEN+consumption%22">OXYGEN consumption</searchLink><br /><searchLink fieldCode="DE" term="%22SCOPOLAMINE%22">SCOPOLAMINE</searchLink><br /><searchLink fieldCode="DE" term="%22ANIMAL+disease+models%22">ANIMAL disease models</searchLink><br /><searchLink fieldCode="DE" term="%22ACTIVE+learning%22">ACTIVE learning</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: 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. [ABSTRACT FROM AUTHOR]
– Name: Abstract
  Label:
  Group: Ab
  Data: <i>Copyright of International Journal of Molecular Sciences is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Text: English
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