电针对肥胖大鼠骨骼肌AMPK/ACC/CPT-1信号通路的影响

目的 观察电针对肥胖大鼠骨骼肌腺苷酸活化蛋白激酶(AMPK)信号通路的影响，探讨电针治疗肥胖的机制。方法 30只刚断乳（3周龄）的SPF级SD雄性大鼠，随机挑选6只普通饲料喂养并设为正常组，另24只高脂饲料喂养造模12周，将造模成功的12只随机分为模型组和电针组。测定各组大鼠体质量、脂肪质量、血脂等相关指标，qPCR检测各组大鼠骨骼肌中AMPKα1、乙酰辅酶A羧化酶(ACC)、肉毒碱棕榈酰转移酶1(CPT-1)的mRNA表达变化， Western blot 法检测骨骼肌AMPK、ACC磷酸化水平和CPT-1蛋白水平。结果 与正常组比较，模型组体质量显著升高（P<0.01），显示肥胖大鼠造模成功。与模型组相比，电针组大鼠的体质量、内脏脂肪质量和血脂均显著降低（P<0.05~0.01）；骨骼肌AMPKα1、ACC、CPT-1 mRNA的表达量显著上升（P<0.05~0.01）。电针使AMPK磷酸化水平显著提高（P<0.01），激活AMPK的活性；ACC磷酸化水平显著提高，抑制ACC活性；同时提高CPT-1蛋白水平。结论 电针可以降低肥胖大鼠的体质量并改善其脂肪代谢的紊乱，其机制可能通过调节骨骼肌组织AMPK/ACC/CPT-1信号通路实现的。 

Effect of Electroacupuncture on AMPK/ACC/CPT-1 Signaling Pathway in Skeletal Muscle of Obese Rats

OBJECTIVE To observe the effect of electroacupuncture (EA) on adenylate-activated protein kinase (AMPK) signal pathway in skeletal muscle of obese rats， and to explore the mechanism of EA treatment for weight loss and fat loss. METHODS 30 SPF SD male rats （3 weeks） were randomly divided into normal group (n=6) and high-fat group (n=24). The model was established by feed on a high fat diet. The obese rats (n=12) were randomly divided into model group (n=6) and EA group (n=6). The body weight， fat weight and serum lipid levels of each group were measured. The levels of AMPKα1， ACC， CPT-1 mRNA expression in skeletal muscle were examined with qPCR. The expression levels of AMPK phosphorylation， ACC phosphorylation and CPT-1 in skeletal muscle were determined by Western blot analysis. RESULTS Compared with the normal group，the body weight of the model group significantly increased， which showed that the model was successfully established. Compared with the model group， the body weight， visceral fat weight and blood lipid of EA group significantly decreased， and the mRNA expression of AMPKα1， ACC and CPT-1 in skeletal muscle in the EA group significantly increased. The phosphorylation levels of AMPK and ACC significantly increased in EA group. Furthermore， the expression level of CPT-1 protein increased in EA group. CONCLUSION EA can reduce the body weight and improve lipid metabolism of obese rats. The mechanism may be related to the regulation of AMPK/ACC/CPT-1 signaling pathway in skeletal muscle.