Mechanisms of electroacupuncture-induced neuroprotection in acute stroke rats: the role of astrocyte-mediated mitochondrial transfer.

IF 8.2 2区 生物学 Q1 CELL BIOLOGY
Yang Guo, Tiancong Fu, Yupei Cheng, Yuxuan Li, Runchen Zhang, Qingtao Ma, Guanran Wang, Wenhua Ning, Wen Fan, Juntao Yang, Mengxiong Zhao, Bohan Liu, Can Wang, Liang Gao, Zhifang Xu, Yi Guo, Xiaoyu Dai, Jiangwei Shi
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引用次数: 0

Abstract

Background: Ischemic stroke significantly threatens human health, and current treatments remain limited, necessitating novel strategies. Mitochondrial transfer between neurons represents a crucial endogenous neuroprotective mechanism.

Objective: This study investigated whether electroacupuncture enhances mitochondrial transfer from astrocytes to damaged neurons during acute cerebral ischemia, promoting neuroprotection.

Methods: A middle cerebral artery occlusion (MCAO) model in Sprague-Dawley (SD) rats and an oxygen-glucose deprivation/reperfusion (OGD/R) model in vitro were employed. Neurobehavioral assessments, electron microscopy, multiplex immunofluorescence, tissue quantification, western blotting, qRT-PCR, transcriptomics, and proteomics were conducted to evaluate mitochondrial distribution, function, and intercellular transfer under electroacupuncture preconditioning and intervention.

Results: Electroacupuncture significantly improved neurological outcomes and reduced brain tissue damage in MCAO rats. It facilitated mitochondrial transfer from astrocytes to neurons, increased functional mitochondria within neurons, and reduced neuronal apoptosis. These effects may involve regulation of the CD38-cADPR-Ca2 + signaling pathway and proteins associated with tunneling nanotubes (TNTs), such as F-actin, Miro1, TRAK1, and KIF5b.

Conclusion: Electroacupuncture enhances mitochondrial transfer and function, exerting neuroprotective effects during acute ischemic stroke. This study highlights the potential of electroacupuncture as a therapeutic approach and identifies novel targets for brain protection strategies.

电针诱导急性脑卒中大鼠神经保护机制:星形胶质细胞介导的线粒体转移的作用。
背景:缺血性脑卒中严重威胁人类健康,目前的治疗仍然有限,需要新的策略。神经元间的线粒体转移是一种重要的内源性神经保护机制。目的:探讨电针是否能促进急性脑缺血时星形胶质细胞向受损神经元的线粒体转移,促进神经保护作用。方法:采用SD大鼠大脑中动脉闭塞(MCAO)模型和体外氧糖剥夺/再灌注(OGD/R)模型。通过神经行为评估、电子显微镜、多重免疫荧光、组织定量、western blotting、qRT-PCR、转录组学和蛋白质组学来评估电针预处理和干预下线粒体分布、功能和细胞间转移。结果:电针可显著改善MCAO大鼠的神经预后,减轻脑组织损伤。它促进了线粒体从星形胶质细胞向神经元的转移,增加了神经元内的功能性线粒体,减少了神经元凋亡。这些影响可能涉及CD38-cADPR-Ca2 +信号通路和与隧道纳米管(TNTs)相关的蛋白质的调节,如F-actin, Miro1, TRAK1和KIF5b。结论:电针可增强急性缺血性脑卒中患者线粒体的转移和功能,发挥神经保护作用。这项研究强调了电针作为一种治疗方法的潜力,并确定了脑保护策略的新靶点。
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来源期刊
CiteScore
11.00
自引率
0.00%
发文量
180
期刊介绍: Cell Communication and Signaling (CCS) is a peer-reviewed, open-access scientific journal that focuses on cellular signaling pathways in both normal and pathological conditions. It publishes original research, reviews, and commentaries, welcoming studies that utilize molecular, morphological, biochemical, structural, and cell biology approaches. CCS also encourages interdisciplinary work and innovative models, including in silico, in vitro, and in vivo approaches, to facilitate investigations of cell signaling pathways, networks, and behavior. Starting from January 2019, CCS is proud to announce its affiliation with the International Cell Death Society. The journal now encourages submissions covering all aspects of cell death, including apoptotic and non-apoptotic mechanisms, cell death in model systems, autophagy, clearance of dying cells, and the immunological and pathological consequences of dying cells in the tissue microenvironment.
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