Electroacupuncture pretreatment alleviates myocardial ischemia/reperfusion-induced lung injury by inhibiting the expression of HMGB1/RAGE in male rats.

IF 2.1 Q3 PHYSIOLOGY

Physiological Reports Pub Date : 2026-09-01 DOI:10.14814/phy2.71066

Chenlong Xie, Jiaojiao Zhang, Yujiao Zhang, Hao Chi, Yue Yong, Jiangang Song

{"title":"Electroacupuncture pretreatment alleviates myocardial ischemia/reperfusion-induced lung injury by inhibiting the expression of HMGB1/RAGE in male rats.","authors":"Chenlong Xie, Jiaojiao Zhang, Yujiao Zhang, Hao Chi, Yue Yong, Jiangang Song","doi":"10.14814/phy2.71066","DOIUrl":null,"url":null,"abstract":"<p><p>Myocardial ischemia-reperfusion (MI/R)-induced lung injury is a major pulmonary complication after cardiac surgery. We aimed to verify this phenomenon in rats and to investigate whether electroacupuncture (EA) pretreatment at bilateral Feishu (BL13) and Zusanli (ST36) acupoints (once daily for 3 days) exerts protective effects. In an MI/R-induced lung injury model in SD rats, EA pretreatment significantly improved lung function and reduced pathological damage (p < 0.05 and p < 0.01, respectively). It also attenuated the pulmonary inflammatory response and decreased the expression of high mobility group box 1 (HMGB1) and receptor for advanced glycation end products (RAGE) (p < 0.05 or p < 0.01). Intratracheal administration of recombinant HMGB1 (rHMGB1) to upregulate lung HMGB1/RAGE signaling impaired the pulmonary protective effect of EA (p < 0.05, p < 0.01). Together, these findings demonstrate that EA pretreatment mitigates MI/R-induced lung injury by inhibiting HMGB1/RAGE signaling.</p>","PeriodicalId":20083,"journal":{"name":"Physiological Reports","volume":"14 18","pages":"e71066"},"PeriodicalIF":2.1000,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13615167/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Physiological Reports","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14814/phy2.71066","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PHYSIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Myocardial ischemia-reperfusion (MI/R)-induced lung injury is a major pulmonary complication after cardiac surgery. We aimed to verify this phenomenon in rats and to investigate whether electroacupuncture (EA) pretreatment at bilateral Feishu (BL13) and Zusanli (ST36) acupoints (once daily for 3 days) exerts protective effects. In an MI/R-induced lung injury model in SD rats, EA pretreatment significantly improved lung function and reduced pathological damage (p < 0.05 and p < 0.01, respectively). It also attenuated the pulmonary inflammatory response and decreased the expression of high mobility group box 1 (HMGB1) and receptor for advanced glycation end products (RAGE) (p < 0.05 or p < 0.01). Intratracheal administration of recombinant HMGB1 (rHMGB1) to upregulate lung HMGB1/RAGE signaling impaired the pulmonary protective effect of EA (p < 0.05, p < 0.01). Together, these findings demonstrate that EA pretreatment mitigates MI/R-induced lung injury by inhibiting HMGB1/RAGE signaling.

查看原文本刊更多论文

电针预处理通过抑制雄性大鼠HMGB1/RAGE的表达减轻心肌缺血/再灌注所致的肺损伤。

心肌缺血再灌注（MI/R）引起的肺损伤是心脏手术后主要的肺部并发症。我们的目的是在大鼠身上验证这一现象，并探讨电针（EA）预处理双侧肺俞穴（BL13）和足三里穴（ST36）（每日1次，连续3天）是否具有保护作用。在心肌梗死/ r致SD大鼠肺损伤模型中，EA预处理可显著改善肺功能，减轻病理损伤(p

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Physiological Reports PHYSIOLOGY-

CiteScore

4.20

自引率

4.00%

发文量

374

审稿时长

9 weeks

期刊介绍： Physiological Reports is an online only, open access journal that will publish peer reviewed research across all areas of basic, translational, and clinical physiology and allied disciplines. Physiological Reports is a collaboration between The Physiological Society and the American Physiological Society, and is therefore in a unique position to serve the international physiology community through quick time to publication while upholding a quality standard of sound research that constitutes a useful contribution to the field.