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[Effects of Electroacupuncture at Neiguan (PC6) on Protein Expressions of Raf-1, ERK 1/2, and p-ERK 1/2 of Rats with Myocardial Hypertrophy].

Objective To observe the effects of electroacupuncture (EA) at Neiguan (PC6) on protein expressions of proto-oncogene serine/threonine-protein kinase-1 ( Raf-1 ) , phospho-extracellular signal-regulated kinase 1/2 (p-ERK 1/2), and extracellular signal-regulated kinase 1/2 (ERK 1/2) in rats with myocardial hypertrophy. Methods Totally 40 healthy Sprague-Dawley (SD) rats of clean grade were divided into 4 groups according to random digit table, i.e., the normal group, the model group, the electroa- cupuncture (EA) group, the sham-EA group, 10 in each group. Rats in the normal group were fed with reg- ular forage. Left ventricular myocardial hypertrophy model was established in rats of the rest 3 groups by subcutaneously injecting isoprinosine hydrochloride (ISO) (at the daily dose of 3 mg/kg) from the nape for a total of 14 days. Rats in the EA group were needed at Neiguan (PC6) using continuous wave (2 Hz, 1 mA, 20-min switching, once per day for 14 days). Rats in the sham-EA group were needled at non-acu- points [5 mm from Neiguan (PC6)] in the same intervention method as the EA group. After intervention ECG was observed and body weight weighed in all rats. Their hearts were removed by open heart surgery and weighed after anesthesia, and then left ventricle were separated and weighed. At last heart weight index (HWI) and left ventricular weight index (LVWI) were calculated. Protein contents of Raf-1 , p-ERK 1/2, and ERK 1/2 in left ventricular myocardial tissue were detected by Western blot. Results Compared with the normal group, elevated ST-segment amplitude, HWI, LVWI, protein expressions of Raf-1 and p-ERK 1/2 were significantly higher in the model group with statistical significance (P <0. 01). Compared with the model group and the sham-EA group, elevated ST-segment amplitude, HWI, LVWI, protein expressions of Raf-1 and p-ERK 1/2 were significantly lower in the EA group with statistical significance (P <0. 05). Conclusion EA could effectively regulate myocardial ischemia in myocardial hypertrophy rats, reduce heart index, and lower protein expressions of Raf-1 and p-ERK 1/2, which might be one of signal regulating mechanisms for EA improving myocardial hypertrophy through Raf/MEK/ERK pathways.