“标本配穴”电针预处理减轻心肌缺血再灌注损伤大鼠心肌细胞铜死亡的机制研究

韦禹岐; 张艳琳; 万小曼; 毛静; 王孙伊; 姜春颜; 曹振阳; 郭倩茹; 吴松

doi:10.13703/j.0255-2930.20250312-0001

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“标本配穴”电针预处理减轻心肌缺血再灌注损伤大鼠心肌细胞铜死亡的机制研究

机制探讨 | 更新时间：2026-09-15

- “标本配穴”电针预处理减轻心肌缺血再灌注损伤大鼠心肌细胞铜死亡的机制研究
- Mechanism of "biaoben acupoint combination" electroacupuncture pretreatment in alleviating cardiomyocyte cuproptosis in rats with myocardial ischemia-reperfusion injury
- 中国针灸 2026年46卷第9期页码：1473-1481
- 作者机构：
  
  湖北中医药大学针灸骨伤学院/针灸治未病湖北省协同创新中心，武汉　430061
  湖北时珍实验室，武汉　430061
  湖北中医药大学附属医院/湖北省中医院针灸科，武汉　430061
- 作者简介：
  
  韦禹岐，湖北中医药大学硕士研究生。E-mail：1589928457@qq.com
  ✉吴松，教授。E-mail：119065124@qq.com
- 基金信息：
  
  2025年湖北省中医药管理局重点项目(ZY2025D001);国家中医药管理局青年岐黄学者培养项目(国中医药人教函〔2022〕256号);国家中医药管理局全国名老中医药专家传承工作室建设项目(国中医药人教函〔2022〕75号)
- DOI：10.13703/j.0255-2930.20250312-0001
  中图分类号：
- 收稿：2025-03-12，
  
  修回：2026-05-27，
  
  网络首发：2026-05-29，
  
  纸质出版：2026-09-12
- 稿件说明：
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韦禹岐, 张艳琳, 万小曼, 等. “标本配穴”电针预处理减轻心肌缺血再灌注损伤大鼠心肌细胞铜死亡的机制研究[J]. 中国针灸, 2026,46(9):1473-1481.

WEI Yuqi, ZHANG Yanlin, WAN Xiaoman, et al. Mechanism of "biaoben acupoint combination" electroacupuncture pretreatment in alleviating cardiomyocyte cuproptosis in rats with myocardial ischemia-reperfusion injury[J]. Chinese Acupuncture & Moxibustion, 2026, 46(9): 1473-1481. DOI: 10.13703/j.0255-2930.20250312-0001.
韦禹岐, 张艳琳, 万小曼, 等. “标本配穴”电针预处理减轻心肌缺血再灌注损伤大鼠心肌细胞铜死亡的机制研究[J]. 中国针灸, 2026,46(9):1473-1481. DOI： 10.13703/j.0255-2930.20250312-0001.

WEI Yuqi, ZHANG Yanlin, WAN Xiaoman, et al. Mechanism of "biaoben acupoint combination" electroacupuncture pretreatment in alleviating cardiomyocyte cuproptosis in rats with myocardial ischemia-reperfusion injury[J]. Chinese Acupuncture & Moxibustion, 2026, 46(9): 1473-1481. DOI: 10.13703/j.0255-2930.20250312-0001. DOI：

摘要

目的：

观察“标本配穴”电针预处理对心肌缺血再灌注损伤（MIRI）大鼠心肌细胞铜死亡的影响，并探讨其作用机制。

方法：

从70只雄性Sprague-Dawley（SD）大鼠中随机选取10只作为假手术（Sham）组，其余大鼠随机分为模型（MIRI）组、伊利司莫（ES）组、“标本配穴”电针预处理（EA）组、“标本配穴”电针预处理+伊利司莫（EA+ES）组，每组15只。EA组和EA+ES组于双侧“内关”、双侧“足三里”和“关元”进行电针预处理，选用连续波，频率2 Hz，每次20 min，每天1次，连续7 d。第8天，除Sham组外，其余组大鼠采用冠状动脉左前降支结扎法建立MIRI模型。术前30 min，ES组和EA+ES组进行腹腔注射铜离子载体elesclomol（5 mg/kg）。造模结束后，TTC染色测定大鼠心肌梗死面积，HE染色观察大鼠缺血区心肌组织形态学，透射电镜观察大鼠缺血区心肌细胞线粒体超微结构，ELISA检测大鼠缺血区心肌细胞线粒体呼吸链复合体表达，Western blot法检测大鼠缺血区心肌细胞铜蓝蛋白（Cp）、铁氧还蛋白1（FDX1）、二氢硫辛酰胺S-琥珀酰转移酶（DLST）、二氢硫辛酰胺S-乙酰转移酶（DLAT）蛋白表达。

结果：

与Sham组比较，MIRI组大鼠心肌梗死面积和缺血区心肌细胞Cp、FDX1、DLST、DLAT蛋白表达升高（

0.01），缺血区心肌细胞线粒体呼吸链复合体Ⅰ-Ⅳ表达降低（

0.01）。与MIRI组比较，EA组大鼠心肌梗死面积和缺血区心肌细胞Cp、FDX1、DLST、DLAT蛋白表达降低（

0.01），缺血区心肌细胞线粒体呼吸链复合体Ⅰ-Ⅳ表达升高（

0.01）；ES组大鼠缺血区心肌细胞Cp和FDX1蛋白表达升高（

0.01）；EA+ES组大鼠缺血区心肌细胞线粒体呼吸链复合体Ⅰ-Ⅳ表达升高（

0.05），缺血区心肌细胞Cp、FDX1、DLST和DLAT蛋白表达降低（

0.01）。与EA组比较，EA+ES组大鼠心肌梗死面积和缺血区心肌细胞Cp、FDX1、DLST和DLAT蛋白表达升高（

0.01，

0.05），缺血区心肌细胞线粒体呼吸链复合体Ⅰ-Ⅳ表达降低（

0.01）。与MIRI组和ES组比较，EA组和EA+ES组大鼠心肌线粒体排列紊乱、线粒体水肿和外膜破裂程度均明显减轻，EA组改善更为明显。

结论：

“标本配穴”电针预处理能够减轻MIRI大鼠心肌细胞及线粒体结构损伤，增强线粒体呼吸链复合体Ⅰ-Ⅳ表达，并通过抑制elesclomol诱导的心肌细胞铜死亡来减轻MIRI。

Abstract

Objective

To observe the effect of "

biaoben

acupoint combination" electroacupuncture (EA) pretreatment on cardiomyocyte cuproptosis in rats with myocardial ischemia-reperfusion injury (MIRI)

and to explore its underlying mechanism.

Methods

From 70 male Sprague-Dawley (SD) rats

10 rats were randomly selected as the sham operation(Sham) group

and the remaining rats were randomly divided into a model (MIRI) group

an elesclomol (ES) group

a "biaoben acupoint combination" EA pretreatment (EA) group

and a "biaoben acupoint combination" EA pretreatment + elesclomol(EA+ES) group

with 15 rats in each group. In the EA group and the EA+ES group

EA pretreatment was applied at bilateral"Neiguan" (PC6)

bilateral "Zusanli" (ST36)

and "Guanyuan" (CV4)

with continuous wave

2 Hz in frequency

20 min each time

once daily for 7 consecutive days. On day 8

except for the Sham group

MIRI model was established by ligation of the left anterior descending branch in the remaining groups. Thirty minutes before modeling

in the ES group and the EA+ES group

intraperitoneal injection of the copper ionophore elesclomol (5 mg/kg) was delivered. After modeling

myocardial infarct area was measured by TTC staining; morphology of cardiomyocytes in the ischemic area was observed by HE staining;mitochondrial ultrastructure of cardiomyocytes in the ischemic area was observed by transmission electron microscopy; the expression of mitochondrial respiratory chain complexes of cardiomyocytes in the ischemic area was detected by ELISA; and the protein expression of ceruloplasmin (Cp)

ferredoxin 1 (FDX1)

dihydrolipoamide S-succinyltransferase (DLST) and dihydrolipoamide S-acetyltransferase (DLAT) of cardiomyocytes in the ischemic area was detected by Western blot.

Results

Compared with the Sham group

the myocardial infarct area and the protein expression of Cp

FDX1

DLST and DLAT of cardiomyocytes in the ischemic area were increased (

0.01)

while the expression of mitochondrial respiratory chain complexes Ⅰ-Ⅳ of cardiomyocytes in the ischemic area was decreased (

0.01) in the MIRI group. Compared with the MIRI group

the myocardial infarct area and the protein expression of Cp

FDX1

DLST and DLAT of cardiomyocytes in the ischemic area were decreased (

0.01)

while the expression of mitochondrial respiratory chain complexes Ⅰ-Ⅳ of cardiomyocytes in the ischemic area was increased (

0.01) in the EA group; the protein expression of Cp and FDX1 of cardiomyocytes in the ischemic area was increased in the ES group (

0.01); the protein expression of Cp

FDX1

DLST and DLAT of cardiomyocytes in the ischemic area was decreased (

0.01)

while the expression of mitochondrial respiratory chain c

omplexes Ⅰ-Ⅳ of cardiomyocytes in the ischemic area was increased (

0.05) in the EA+ES group. Compared with the EA group

the myocardial infarct area and the protein expression of Cp

FDX1

DLST and DLAT were increased (

0.01

0.05)

while the expression of mitochondrial respiratory chain complexes Ⅰ-Ⅳ of cardiomyocytes in the ischemic area was decreased (

0.01) in the EA+ES group. Compared with the MIRI group and the ES group

in the EA group and the EA+ES group

disordered arrangement of myocardial mitochondria

mitochondria edema

and mitochondrial outer membrane rupture were improved

the improvement in the EA group was more pronounced.

Conclusion

Biaoben

acupoint combination" EA pretreatment can attenuate the structural damage of cardiomyocytes and mitochondria

enhance the expression of mitochondrial respiratory chain complexes Ⅰ-Ⅳ in MIRI rats

and alleviate MIRI by inhibiting elesclomol-induced cardiomyocyte cuproptosis.

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