Enriched environment treatment promotes neurofunctional recovery by regulating the ALK5/Smad2/3/Gadd45β signaling pathway in rats with cerebral ischemia /reperfusion injury.

Autor: Liu G; Department of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Electronic address: 2021110343@stu.cqmu.edu.cn., Xie C; Department of Neurology, Affiliated Hospital & Clinical Medical College of Chengdu University, Chengdu, Sichuan Province, China; Chongqing Key Laboratory of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Electronic address: xiechenchen-888@163.com., Li J; Department of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China. Electronic address: 623929204@qq.com., Jiang X; Department of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Electronic address: 493018442@qq.com., Tang H; Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Electronic address: 2022140024@stu.cqmu.edu.cn., Li C; Department of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China. Electronic address: licq@cqmu.edu.cn., Zhang K; School of Clinical Medicine, Chongqing Medical and Pharmaceutical College, Chongqing, China. Electronic address: 11006@cqmpc.edu.cn.
Jazyk: angličtina
Zdroj: Neurochemistry international [Neurochem Int] 2024 Sep; Vol. 178, pp. 105806. Date of Electronic Publication: 2024 Jul 18.
DOI: 10.1016/j.neuint.2024.105806
Abstrakt: It has been demonstrated that an enriched environment (EE) treatment can alter neuroplasticity in neurodegenerative diseases. However, the role of EE treatment in ischemic stroke remains unclear. Previous findings have revealed that EE treatment can promote cerebral activin-receptor-like-kinase-5 (ALK5) expression after cerebral ischemia/reperfusion (I/R) injury. ALK5 has been identified as a potential mediator of neuroplasticity through its modulation of Smad2/3 and Gadd45β. Therefore, the aim of this study was to investigate whether EE treatment could promote neurofunctional recovery by regulating the ALK5/Smad2/3/Gadd45β pathway. The study utilized the rat model of middle cerebral artery occlusion/reperfusion (MCAO/R). The ALK5/Smad2/3/Gadd45β signaling pathway changes were evaluated using western blotting (WB). Brain injury was assessed by infarct volume and neurobehavioral scores. The effect of EE treatment on neurogenesis was evaluated using Doublecortin (DCX) and Nestin, axonal plasticity with biotinylated dextran amine (BDA) nerve tracing, and dendritic plasticity was assessed using Golgi-Cox staining. EE treatment has been demonstrated to modulate the Smad2/3/Gadd45β pathway by regulating the expression of ALK5. The protective effects of EE treatment on brain infarct volume, neurological function, newborn neurons, dendritic and axonal plasticity following cerebral I/R injury were counteracted by ALK5 silencing. EE treatment can enhance neurofunctional recovery after cerebral I/R injury, which is achieved by regulating the ALK5/Smad2/3/Gadd45β signaling pathway to promote neuroplasticity.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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