安普克
过剩4
信号转导
神经科学
线粒体
功能(生物学)
医学
生物
内分泌学
内科学
细胞生物学
糖尿病
胰岛素抵抗
磷酸化
蛋白激酶A
作者
Xinyue Wu,Chen Li,Changkai Ke,Chuan Huang,Bingchen Pan,Chunxiao Wan,Chunxiao Wan
出处
期刊:Neuroreport
[Lippincott Williams & Wilkins]
日期:2024-05-15
卷期号:35 (10): 648-656
被引量:8
标识
DOI:10.1097/wnr.0000000000002048
摘要
Mitochondria play a crucial role in maintaining cellular energy supply and serve as a source of energy for repairing nerve damage following a stroke. Given that exercise has the potential to enhance energy metabolism, investigating the impact of exercise on mitochondrial function provides a plausible mechanism for stroke treatment. In our study, we established the middle cerebral artery occlusion (MCAO) model in Sprague–Dawley rats and implemented early exercise intervention. Neurological severity scores, beam-walking test score, and weight were used to evaluate neurological function. The volume of cerebral infarction was measured by MRI. Nerve cell apoptosis was detected by TUNEL staining. Mitochondrial morphology and structure were detected by mitochondrial electron microscopy. Mitochondrial function was assessed using membrane potential and ATP measurements. Western blotting was used to detect the protein expression of AMPK/PGC-1α/GLUT4. Through the above experiments, we found that early exercise improved neurological function in rats after MCAO, reduced cerebral infarction volume and neuronal apoptosis, promoted the recovery of mitochondrial morphology and function. We further examined the protein expression of AMPK/PGC-1α/GLUT4 signaling pathway and confirmed that early exercise was able to increase its expression. Therefore, we suggest that early exercise initiated the AMPK/PGC-1α/GLUT4 signaling pathway, restoring mitochondrial function and augmenting energy supply. This, in turn, effectively improved both nerve and body function in rats following ischemic stroke.
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