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Preliminary Study of β1-Adrenergic Receptor and M2 Muscarinic Cholinergic Receptor Mediated Protective Effect of Electroacupuncture on PC6 against Myocardial Ischemia

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The aims of the present study were to observe the effect of electroacupuncture (EA) at Neiguan (PC6) on ischemic myocardium and the involvement of myocardial β1-adrenergic (β1AR) and M2 cholinergic muscarinic receptors (M2AChR) in the protective effect. The C57BL6 mice were divided into control, model and PC6 groups randomly. The myocardial ischemia (MI) model of mice was established by forced exhaustive swimming (ES). EA at PC6 was performed to the PC6 group for 7 days. The Electrocardiograph (ECG) was recorded before ES and immediately after ES on the 1st and 7th day. The ECG J-point deviation value and heart rate (HR) were analyzed to evaluate the effect of EA. The β1AR and M2AChR knockout mice were used to explore whether β1AR and M2AChR in the cardiac myocytes mediated the cardioprotection effect of EA. The β1AR knockout (β1AR-/-) and M2AChR knockout (M2AChR-/-) mice were divided into MI model and PC6 groups respectively and treated the same way corresponding to the groups of C57BL6 mice. The results showed that the Electrocardiograph (ECG) J-point deviation value in C57BL6 mice were significantly increased after MI (P=0.015 in the model group, P=0.001 in the PC6 group), which is a symptom of MI, while the heart rate (HR) on the 1st decreased significantly (P<0.05, or P<0.01). Following EA in the C57BL6 mice, the J-point deviation on the 7th day was significantly decreased (P=0.031, decreased 70.05%), but the HR was still much slower than their baseline (both P<0.01). The increased J-point deviation value and decreased HR level were also observed in both β1AR-/- and M2AChR-/- mice (P<0.05, or P<0.01). While no significant changes were found in the J point deviation after EA intervention on the 7th day, and in HR of the both types of mice. These results suggested that EA at PC6 could protect the myocardium against ischemic injury, probably mediated by myocardial β1AR and M2AChR.
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Document Type: Research Article

Publication date: December 14, 2017

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