OBJECTIVE: To observe the effect of electroacupuncture (EA) stimulation of "Neiguan" (PC 6) on expression of sodium (Nav) channel α-subunit 1.5 and Nav β-subunits β 1-β 4 (the known myocardial sodium channel proteins) in acute myocardial ischemia (AMI) rats so as to explore its mechanisms underlying protection of ischemic myocardium. METHODS: Sixty SD male rats were randomly divided into normal control, AMI model, Neiguan (PC 6), Lieque (LU 7) and non-acupoint groups. The AMI model was established by intravenous injection of Isoprenaline (85 mg/kg) once daily for 2 days. Myocardial Nav 1.5 and Nav β 1, β 2, β 3, β 4 protein expression levels were detected by Western blot. RESULTS: In comparison with the control group, myocardial Nav 1.5, β 1, β 2, β 3 and β 4 protein expression levels were significantly down-regulated in the AMI model group (P<0.01). After EA stimulation, compared with the model group, the expression levels of Nav 1.5, Nav β 1, β 2, β 3 and β 4 protein expression levels were significantly up-regulated in the Neiguang (PC 6) and Lieque (LU 7) groups (P<0.01) rather than in the non-acupoint group (P>0.05). There was no statistical significance between the Neiguan (PC 6) and Lieque (LU 7) groups in β 4 protein expression level (P>0.05). CONCLUSION: EA stimulation of both PC 6 and LU 7 can significantly reverse AMI-induced down-regulation of myocardial Nav 1.5, β 1, β 2, β 3 and β 4 protein expression levels in AMI rats, which might contribute to its function in improving AMI by reducing calcium overload.
OBJECTIVE: To observe the effect of electroacupuncture (EA) stimulation of "Neiguan" (PC 6) on expression of sodium (Nav) channel α-subunit 1.5 and Nav β-subunits β 1-β 4 (the known myocardial sodium channel proteins) in acute myocardial ischemia (AMI) rats so as to explore its mechanisms underlying protection of ischemic myocardium. METHODS: Sixty SD male rats were randomly divided into normal control, AMI model, Neiguan (PC 6), Lieque (LU 7) and non-acupoint groups. The AMI model was established by intravenous injection of Isoprenaline (85 mg/kg) once daily for 2 days. Myocardial Nav 1.5 and Nav β 1, β 2, β 3, β 4 protein expression levels were detected by Western blot. RESULTS: In comparison with the control group, myocardial Nav 1.5, β 1, β 2, β 3 and β 4 protein expression levels were significantly down-regulated in the AMI model group (P<0.01). After EA stimulation, compared with the model group, the expression levels of Nav 1.5, Nav β 1, β 2, β 3 and β 4 protein expression levels were significantly up-regulated in the Neiguang (PC 6) and Lieque (LU 7) groups (P<0.01) rather than in the non-acupoint group (P>0.05). There was no statistical significance between the Neiguan (PC 6) and Lieque (LU 7) groups in β 4 protein expression level (P>0.05). CONCLUSION: EA stimulation of both PC 6 and LU 7 can significantly reverse AMI-induced down-regulation of myocardial Nav 1.5, β 1, β 2, β 3 and β 4 protein expression levels in AMIrats, which might contribute to its function in improving AMI by reducing calcium overload.