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Updated: Feb 6, 2026

Acute Myocardial Infarction in Rats
Published on: February 16, 2011
[Effect of Electroacupuncture on Hippocampal IL-6, IL-1 β, TNF-α and Norepinephrine Levels in Acute Myocardial
Kun Wang1, Sheng-Bing Wu2, Shuai Cui3
1Graduate School, Anhui University of Traditional Chinese Medicine, Hefei 230038, China.
Objective:
We have repeatedly demonstrated that electroacupuncture (EA) stimulation of "Shenmen" (HT 7)- "Tongli" (HT 5) segment of the Heart Meridian can improve acute myocardial ischemia (AMI). This study aimed at observing the effect of EA on contents of hippocampal norepinephrine (NE), and interleukin 6 (IL-6), IL-1 β and tumor necrosis factor- α (TNF-α) in AMI rats, so as to explore its underlying mechanism.
Methods:
SD rats were randomly divided into 3 groups: sham operation (sham), model and EA(n=6 rats in each). The anterior descending branch (ADB) of the left coronary artery was occluded to make an AMI model. For rats of the sham group, a surgical suture was simply threaded beneath the ADB without ligation. EA (2 Hz/15 Hz, 1 mA) was applied to bilateral "Shenmen" (HT 7)- "Tongli" (HT 5) and the middle-point between HT 7 and HT 5 for 30 min, once daily for 3 days. Electrocardiogram (ECG) of the neck-thoracic lead was recorded by using PowerLab 16. The contents of serum creatine kinase (CK), hippocampal IL-6, IL-1 β and TNF-α were assayed by ELISA. The concentration of NE in hippocampal CA 1 area was detected by microdialysis combined with electrochemical detector.
Results:
Compared with the sham group, the ECG-ST height, serum CK, hippocampal NE, IL-6, IL-1 β and TNF-α contents of the CA 1 region were significantly increased in the model group (P<0.001). Whereas, after EA intervention, the serum CK, hippocampal NE, IL-6, IL-1 β and TNF-α contents were obviously down-regulated relevant to the model group (P<0.05, P<0.001), and the IL-6, IL-1 β and TNF-α contents were positively correlated with the NE level (P<0.001, P<0.01).
Conclusion:
EA stimulation of the Heart Meridian may improve ischemic myocardial injury in AMI rats, probably by reducing the proinflammatory factors and hippocampal NE.
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