ABSTRACT
OBJECTIVE: To observe the effect of electroacupuncture(EA) on expression of phosphorylated (pAkt) and caspase-3 proteins in the skeletal muscle in mice with diabetes, so as to provide experimental evidence for treating diabetic myopathy in clinic. METHODS: Eighteen C 57 mice were equally randomized into control, model and EA groups (n = 6 mice/ group). Type 1 diabetic model was established by streptozotocin (STZ, i. P., 200 mg/kg). EA (1 mA, 20-30 Hz) was applied to bilateral "Zusanli"(ST 36) and "Yanglingquan" (GB 34) for 20 min, once daily for 14 days. Damp weights of the musculus soleus, plantaris, gastrocnemius, extensor digitorum longus and tibialis anterior were measured, and Western blot was used to measure the expression levels of pAkt (ser 473), pAkt(Thr 308), total Akt and caspase-3 proteins in the aforementioned skeleton muscles. RESULTS: Compared with the normal control group, the weights of the musculus soleus, plantaris, gastrocnemius, extensor digitorum longus and tibialis anterior were decreased obviously in the model group (P < 0.01). After EA treatment, the weights of the 5 skeleton muscles were all increased apparently compared with the model group (P < 0.05). In comparison with the normal control group, muscular pAkt (Thr 308) protein expression level was down-regulated significantly in the model group (P < 0.01), while that of muscular caspase-3 protein expression of the model group was up-regulated considerably (P < 0.01). Following EA, the expression levels of muscular pAkt (Thr 308) and pAkt (ser 473) in the EA group were upregulated apparently (P < 0.01), while that of muscular caspase-3 protein was down-regulated obviously (P < 0.01). No significant differences were found between the control and model groups in the expression levels of muscular pAkt (ser 473) and total Akt proteins (P > 0.05). CONCLUSION: EA intervention can effectively up-regulate expression of pAkt (Thr 308 and ser 473) and down-regulate expression of caspase-3 protein in the skeleton muscle in diabetic mice, which may contribute to its effect in inhibiting diabetic myopathy.
