Wang Wei, Li Ji-Quan, Meng Xiang-Yu, Chen Yi-Guo, Jing Qin
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2017 Apr;37(4):448-452.
Objective To observe the effect of electroacupuncture (EA) at different acupoints on mRNA expressions of ATP-sensitive potassium channel (Kir6. 1, Kir6. 2) and conjugated protein (SUR2A, SUR2B) and protein kinases (PKA, PKG and PKC132) in myocardial ischemia model rats. Methods Myocardial ischemia model was established in healthy male SD rats via subcutaneously injec- ting ISO (85 mg/kg) multipointedly (medial root of limbs and the back). Then they were randomly divided into 4 groups, i.e., the model group, Neiguan (PC6) group, Lieque (LU7) group, non-acupoint group, 10 in each group. Besides, another 10 healthy rats were recruited as the control group. Corresponding EA was performed at respective acupoints to rats in Neiguan (PC6) group, Lieque (LU7) group, non-acu- point group, with dense-sparse wave, 2 -3 mA, 2 -20 Hz, needle retaining time of 20 min, once per day for 7 successive days. mRNA expression levels of Kir6. 1 and Kir6. 2, SUR2A, SUR2B, PKA, PKG, and PKCβ₂ in left ventricular myocardium were analyzed by Real-time PCR. Results Compared with the con- trol group, mRNA expressions of each index increased in the model group (P <0. 01). Compared with the model group, mRNA expressions of each index significantly decreased in Neiguan (PC6) group and Lieque (LU7) group (P<0. 01). Compared with Neiguan (PC6) group, mRNA expressions of each index significantly increased in Lieque (LU7) group and non-acupoint group (P <0. 01). Compared with Lieque (LU7) group, mRNA expressions of each index significantly increased in non-acupoint group (P <0. 05). Conclusion EA at Neiguan (PC6) could reverse mRNA expression changes of ATP-sensitive potassium channel (Kir6. 1 and Kir6. 2)and conjugated proteins (SUR2A and SUR2B) and protein kinases (PKA, PKG, and PKCβ₂).
目的 观察电针不同穴位对心肌缺血模型大鼠三磷酸腺苷敏感性钾通道（Kir6.1、Kir6.2）、结合蛋白（SUR2A、SUR2B）及蛋白激酶（PKA、PKG和PKCβ₂）mRNA表达的影响。方法 将健康雄性SD大鼠通过多点皮下注射异丙肾上腺素（ISO，85 mg/kg）（四肢内侧根部及背部）建立心肌缺血模型。然后将其随机分为4组，即模型组、内关（PC6）组、列缺（LU7）组、非穴位组，每组10只。另取10只健康大鼠作为对照组。对内关（PC6）组、列缺（LU7）组、非穴位组大鼠分别在相应穴位进行电针治疗，采用疏密波，2～3 mA，2～20 Hz，留针时间20 min，每天1次，连续7天。采用实时荧光定量PCR法分析左心室心肌中Kir6.1、Kir6.2、SUR2A、SUR2B、PKA、PKG及PKCβ₂的mRNA表达水平。结果 与对照组比较，模型组各指标mRNA表达均升高（P<0.01）。与模型组比较，内关（PC6）组和列缺（LU7）组各指标mRNA表达均显著降低（P<0.01）。与内关（PC6）组比较，列缺（LU7）组和非穴位组各指标mRNA表达均显著升高（P<0.01）。与列缺（LU7）组比较，非穴位组各指标mRNA表达显著升高（P<0.05）。结论 电针内关（PC6）可逆转三磷酸腺苷敏感性钾通道（Kir6.1和Kir6.2）、结合蛋白（SUR2A和SUR2B）及蛋白激酶（PKA、PKG和PKCβ₂）的mRNA表达变化。
