PDF(Pubmed)
Abstract：
UNASSIGNED: Electroacupuncture (EA) has been demonstrated to aid stroke recovery. However, few investigations have focused on identifying the potent molecular targets of EA by comparing EA stimulation between naïve and disease models. Therefore, this study was undertaken to identify the potent molecular therapeutic mechanisms underlying EA stimulation in ischemic stroke through a comparison of mRNA sequencing data obtained from EA-treated naïve control and ischemic stroke mouse models.
UNASSIGNED: Using both naïve control and middle cerebral artery occlusion (MCAO) mouse models, EA stimulation was administered at two acupoints, Baihui (GV20) and Dazhui (GV14), at a frequency of 2 Hz. Comprehensive assessments were conducted, including behavioral evaluations, RNA sequencing to identify differentially expressed genes (DEGs), functional enrichment analysis, protein-protein interaction (PPI) network analysis, and quantitative real-time PCR.
UNASSIGNED: EA stimulation ameliorated the ischemic insult-induced motor dysfunction in mice with ischemic stroke. Comparative analysis between control vs. MCAO, control vs. control + EA, and MCAO vs. MCAO + EA revealed 4,407, 101, and 82 DEGs, respectively. Of these, 30, 7, and 1 were common across the respective groups. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses revealed upregulated DEGs associated with the regulation of inflammatory immune response in the MCAO vs. MCAO + EA comparison. Conversely, downregulated DEGs in the control vs. control + EA comparison were linked to neuronal development. PPI analysis revealed major clustering related to the regulation of cytokines, such as Cxcl9, Pcp2, Ccl11, and Cxcl13, in the common DEGs of MCAO vs. MCAO + EA, with Esp8l1 identified as the only common downregulated DEG in both EA-treated naïve and ischemic models.
UNASSIGNED: These findings underscore the diverse potent mechanisms of EA stimulation between naïve and ischemic stroke mice, albeit with few overlaps. However, the potent mechanisms underlying EA treatment in ischemic stroke models were associated with the regulation of inflammatory processes involving cytokines.
UNASSIGNED: Using both naïve control and middle cerebral artery occlusion (MCAO) mouse models, EA stimulation was administered at two acupoints, Baihui (GV20) and Dazhui (GV14), at a frequency of 2 Hz. Comprehensive assessments were conducted, including behavioral evaluations, RNA sequencing to identify differentially expressed genes (DEGs), functional enrichment analysis, protein-protein interaction (PPI) network analysis, and quantitative real-time PCR.
UNASSIGNED: EA stimulation ameliorated the ischemic insult-induced motor dysfunction in mice with ischemic stroke. Comparative analysis between control vs. MCAO, control vs. control + EA, and MCAO vs. MCAO + EA revealed 4,407, 101, and 82 DEGs, respectively. Of these, 30, 7, and 1 were common across the respective groups. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses revealed upregulated DEGs associated with the regulation of inflammatory immune response in the MCAO vs. MCAO + EA comparison. Conversely, downregulated DEGs in the control vs. control + EA comparison were linked to neuronal development. PPI analysis revealed major clustering related to the regulation of cytokines, such as Cxcl9, Pcp2, Ccl11, and Cxcl13, in the common DEGs of MCAO vs. MCAO + EA, with Esp8l1 identified as the only common downregulated DEG in both EA-treated naïve and ischemic models.
UNASSIGNED: These findings underscore the diverse potent mechanisms of EA stimulation between naïve and ischemic stroke mice, albeit with few overlaps. However, the potent mechanisms underlying EA treatment in ischemic stroke models were associated with the regulation of inflammatory processes involving cytokines.
摘要：
■电针（EA）已被证明可以帮助中风恢复。然而,很少有研究集中在通过比较初治和疾病模型之间的EA刺激来确定EA的有效分子靶标。因此,本研究通过比较EA治疗的初始对照和缺血性卒中小鼠模型的mRNA测序数据,确定EA刺激缺血性卒中的有效分子治疗机制.
■使用幼稚对照和大脑中动脉闭塞（MCAO）小鼠模型，在两个穴位进行EA刺激，百汇（GV20）和大竹（GV14），频率为2Hz。进行了全面评估，包括行为评估，RNA测序以鉴定差异表达基因(DEGs)，功能富集分析，蛋白质-蛋白质相互作用（PPI）网络分析，和定量实时PCR。
■EA刺激改善了缺血性中风小鼠的缺血性损伤诱导的运动功能障碍。对照与对照之间的比较分析MCAO,控制vs.control+EA,和MCAOvs.MCAO+EA显示4,407,101和82个DEG,分别。其中,30、7和1在各组中是共同的。基因本体论（GO）和京都基因和基因组百科全书（KEGG）途径分析揭示了上调的DEGs与MCAO中炎症免疫反应的调节有关MCAO+EA比较。相反，控制中下调的DEG与对照+EA比较与神经元发育有关。PPI分析显示与细胞因子调节相关的主要聚类，例如Cxcl9、Pcp2、Ccl11和Cxcl13，在MCAO的常见DEG与MCAO+EA,Esp8l1被确定为EA处理的幼稚和缺血模型中唯一常见的下调DEG。
■这些发现强调了初治和缺血性中风小鼠之间EA刺激的不同有效机制，尽管重叠很少。然而,在缺血性卒中模型中,EA治疗的有效机制与细胞因子对炎症过程的调节相关.
■使用幼稚对照和大脑中动脉闭塞（MCAO）小鼠模型，在两个穴位进行EA刺激，百汇（GV20）和大竹（GV14），频率为2Hz。进行了全面评估，包括行为评估，RNA测序以鉴定差异表达基因(DEGs)，功能富集分析，蛋白质-蛋白质相互作用（PPI）网络分析，和定量实时PCR。
■EA刺激改善了缺血性中风小鼠的缺血性损伤诱导的运动功能障碍。对照与对照之间的比较分析MCAO,控制vs.control+EA,和MCAOvs.MCAO+EA显示4,407,101和82个DEG,分别。其中,30、7和1在各组中是共同的。基因本体论（GO）和京都基因和基因组百科全书（KEGG）途径分析揭示了上调的DEGs与MCAO中炎症免疫反应的调节有关MCAO+EA比较。相反，控制中下调的DEG与对照+EA比较与神经元发育有关。PPI分析显示与细胞因子调节相关的主要聚类，例如Cxcl9、Pcp2、Ccl11和Cxcl13，在MCAO的常见DEG与MCAO+EA,Esp8l1被确定为EA处理的幼稚和缺血模型中唯一常见的下调DEG。
■这些发现强调了初治和缺血性中风小鼠之间EA刺激的不同有效机制，尽管重叠很少。然而,在缺血性卒中模型中,EA治疗的有效机制与细胞因子对炎症过程的调节相关.
