电针内关穴对肥厚心肌细胞JNK信号通路的影响

Effects of Electroacupuncture at Neiguan(PC6) on c-Jun NH2-teminal Kinase Signaling Pathways in Hypertrophic Myocardial Cells

目的探讨电针内关穴对心肌肥厚(cardiac hypertrophy,CH)模型大鼠心肌细胞c-Jun氨基末端激酶(c-Jun NH2-teminal kinase,JNK)信号通路的影响。方法 30只SD雌性大鼠随机分为正常组、模型组和电针组,每组10只。模型组和电针组以盐酸异丙肾上腺素3mg/(kg·d)背部皮下注射14天的方法制备CH大鼠模型;正常组注射等量生理盐水。电针组在造模的同时选取内关穴进行电针,每天1次,共14天。计算各组大鼠左心室质量指数(left ventricula rweight index,LVWI)和全心质量指数(heart weight index,HWI);采用放射免疫法检测心肌组织血管紧张素Ⅱ(AngⅡ)含量;免疫印迹法检测心肌细胞JNK和磷酸化JNK(p-JNK)蛋白表达。结果与正常组比较,模型组大鼠LVWI、HWI升高,左心室AngⅡ含量增加,JNK及p-JNK表达升高,差异均有统计学意义(P<0.01)。电针组上述指标均明显低于模型组,差异有统计学意义(P<0.05)。结论电针内关穴防治CH与调节JNK信号通路有关;电针可能是通过调节其上游神经内分泌因子来发挥作用。

Objective To study the effects of electroacupuncture （EA） at Neiguan （PC6） on c-Jun NH2- terminal kinases （JNK） signaling pathways in hypertrophic myocardial cells. Methods Thirty female SD rats were randomly divided into three groups, i. e., the normal group, the model group, and the EA group, 10 in each group. Isoprenaline hydrochloride （ISO） injection at the daily dose of 3 mg/kg was subcutaneously injected for 14 days to establish the cardiac hypertrophy （CH） model. Rats in normal group were subcutaneously injected with an equal volume of normal saline. EA at Neiguan （PC6） was applied for rats in the EA group while model- ing, once daily, for 14 successive days. The left ventricular weight index （LVWl） and heart weight index （HWl） were calculated in all rats. The content of angiotensin II （Ang II ） in the cardiac muscular tissue was tested using radioimmunoassay. The protein expressions of JNK and phosphorated JNK （p-JNK） in cardiocytes were detec- ted using Western blot. Results Compared with the normal group, LVWl and HWl, the Ang II content, and the expressions of JNK and p-JNK were significantly higher in the model group, showing statistical difference （ P 〈 0.01 ）. The aforesaid indices were obviously lower in the EA group than in the model group with statistical differ- ence （ P 〈0.05）. Conclusions EA at PC6 could prevent and treat CH possibly correlated with regulation of JNK signaling pathways. EA might play a role possibly through regulating its upstream neuroendocrine factors.