Fan Xiaofang, Guo Wei, Yang Xiaodan, Zhang Hao, Fink Bruno, Hu Lingyu, Wang Xiaoguang
Faculty of Graduate Studies, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, China.
Department of Surgery, The Second Affiliated Hospital of Jiaxing University, Jiaxing 314000, Zhejiang, China.
Mediators Inflamm. 2025 Aug 30;2025:4932970. doi: 10.1155/mi/4932970. eCollection 2025.
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（EA）已在大鼠模型中显示出对肝缺血再灌注损伤（HIRI）的保护作用。本研究旨在探讨EA对HIRI发挥保护作用的潜在分子机制。分析了来自基因表达综合数据库（GEO）的基因表达微阵列数据，以鉴定与HIRI相关的基因，随后进行差异表达分析。我们的结果显示，EA治疗显著降低了血清丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST）水平，以及肝组织中的髓过氧化物酶（MPO）活性。组织学分析表明，EA治疗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表达并抑制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通过靶向Esr1/TAK1-JNK/p38信号通路，是减轻HIRI的一种有效治疗方法。
