Exercise training alleviates neuronal apoptosis and re-establishes mitochondrial quality control after cerebral ischemia by increasing SIRT3 expression.

Publisher: Springer Country of Publication: Switzerland NLM ID: 8506639 Publication Model: Electronic Cited Medium: Internet ISSN: 1573-6822 (Electronic) Linking ISSN: 07422091 NLM ISO Abbreviation: Cell Biol Toxicol Subsets: MEDLINE

Publication: [Cham] : Springer
Original Publication: Princeton, N.J. : Princeton Scientific Publishers, c1984-

Sirtuin 3*/metabolism ; Sirtuin 3*/genetics ; Apoptosis* ; Brain Ischemia*/metabolism ; Mitochondria*/metabolism ; Physical Conditioning, Animal*/physiology ; Neurons*/metabolism ; Neurons*/pathology ; Rats, Sprague-Dawley*; Animals ; Male ; Rats ; Mitophagy/physiology ; Mitochondrial Dynamics/physiology ; Sirtuins

Existing evidence indicates that exercise training can enhance neural function by regulating mitochondrial quality control (MQC), which can be impaired by cerebral ischemia, and that sirtuin-3 (SIRT3), a protein localized in mitochondria, is crucial in maintaining mitochondrial functions. However, the relationship among exercise training, SIRT3, and MQC after cerebral ischemia remains obscure. This study attempted to elucidate the relationship among exercise training, SIRT3 and MQC after cerebral ischemia in rats. Male adult SD rats received tMCAO after the transfection of adeno-associated virus encoding either sirtuin-3 (AAV-SIRT3) or SIRT3 knockdown (AAV-sh-SIRT3) into the ipsilateral striata and cortex. Subsequently, the animals were randomly selected for exercise training. The index changes were measured by transmission electron microscopy, Western blot analysis, nuclear magnetic resonance imaging, TUNEL staining, and immunofluorescence staining, etc. The results revealed that after cerebral ischemia, exercise training increased SIRT3 expression, significantly improved neural function, alleviated infarct volume and neuronal apoptosis, maintained the mitochondrial structural integrity, and re-established MQC. The latter promoted mitochondrial biogenesis, balanced mitochondrial fission/fusion, and enhanced mitophagy. These favorable benefits were reversed after SIRT3 interference. In addition, a cellular OGD/R model showed that the increased SIRT3 expression alleviates neuronal apoptosis and re-establishes mitochondrial quality control by activating the β-catenin pathway. These findings suggest that exercise training may optimize mitochondrial quality control by increasing the expression of SIRT3, thereby improving neural functions after cerebral ischemia, which illuminates the mechanism underlying the exercise training-conferred neural benefits and indicates SIRT3 as a therapeutic strategy for brain ischemia.
Competing Interests: Declarations. Competing Interests: The authors declare no competing interests. Ethical Approval: The protocols adhered to the National Institute of Health guidelines (NIH Publications NO. 80–23, revised 1996). Approval for this experiment was obtained from the Institutional Animal Care and Use Committee (IACUC) of Fujian Medical University, Fujian, China [Approval No. 20220603].
(© 2024. The Author(s).)

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No. 2023QH2026 Startup Fund for Scientific Research, Fujian Medical University; 2021Y9060 Joint Funds for the innovation of science and Technology, Fujian province; No. 2022XH026 Excellent Young Scholars Cultivation Project of Fujian Medical University Union Hospital; No. 81802225 National Natural Science Foundation of China

Keywords: Cerebral ischemia; Exercise training; Mitochondrial Quality Control (MQC); Neuronal apoptosis; SIRT3

EC 3.5.1.- (Sirtuin 3)
0 (SIRT3 protein, rat)
EC 3.5.1.- (Sirtuins)

Date Created: 20241220 Date Completed: 20241220 Latest Revision: 20241220

20241222

10.1007/s10565-024-09957-3

39707047