Electroacupuncture Attenuates Hepatic Ischemia-Reperfusion Injury by Modulating the Esr1/TAK1-JNK/p38 Signaling Pathway in Rats.

IF 4.2 3区 医学 Q2 CELL BIOLOGY
Mediators of Inflammation Pub Date : 2025-08-30 eCollection Date: 2025-01-01 DOI:10.1155/mi/4932970
Xiaofang Fan, Wei Guo, Xiaodan Yang, Hao Zhang, Bruno Fink, Lingyu Hu, Xiaoguang Wang
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引用次数: 0

Abstract

Electroacupuncture (EA) has demonstrated protective effects against hepatic ischemia-reperfusion injury (HIRI) in rat models. This study aimed to explore the underlying molecular mechanisms by which EA exerts its protective effects against HIRI. Gene expression microarray data from the Gene Expression Omnibus (GEO) database were analyzed to identify genes associated with HIRI, followed by differential expression analysis. Our results revealed that EA treatment significantly reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, as well as myeloperoxidase (MPO) activity in liver tissues. Histological analysis indicated decreased necrotic areas and apoptosis in EA-treated liver tissues. Molecular assessments demonstrated that EA downregulated Esr1 expression and inhibited the activation of the TAK1-JNK/p38 signaling pathway, thereby reducing hepatocyte apoptosis and inflammatory responses. These findings suggest that EA serves as a potent therapeutic approach to alleviate HIRI by targeting the Esr1/TAK1-JNK/p38 signaling pathway.

电针通过调节Esr1/TAK1-JNK/p38信号通路减轻大鼠肝缺血再灌注损伤
电针(EA)对大鼠肝缺血再灌注损伤(HIRI)具有保护作用。本研究旨在探讨EA对HIRI发挥保护作用的潜在分子机制。分析来自基因表达综合数据库(GEO)的基因表达微阵列数据,确定与HIRI相关的基因,然后进行差异表达分析。我们的研究结果显示,EA治疗显著降低血清谷丙转氨酶(ALT)和天冬氨酸转氨酶(AST)水平,以及肝组织髓过氧化物酶(MPO)活性。组织学分析显示,经ea处理的肝组织坏死面积和细胞凋亡减少。分子评估表明,EA下调Esr1表达,抑制TAK1-JNK/p38信号通路的激活,从而减少肝细胞凋亡和炎症反应。这些发现表明,EA可作为一种有效的治疗方法,通过靶向Esr1/TAK1-JNK/p38信号通路来缓解HIRI。
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来源期刊
Mediators of Inflammation
Mediators of Inflammation 医学-免疫学
CiteScore
8.70
自引率
0.00%
发文量
202
审稿时长
4 months
期刊介绍: Mediators of Inflammation is a peer-reviewed, Open Access journal that publishes original research and review articles on all types of inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, leukotrienes, PAF, biological response modifiers and the family of cell adhesion-promoting molecules.
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