电针对自发性高血压大鼠心肌肥厚的影响

Effects of Electroacupuncture on Cardiac Hypertrophy of Spontaneously Hypertensive Rats

目的探讨电针治疗高血压病合并心肌肥厚的可能作用机制。方法将12周龄雄性WKY大鼠12只作为正常组,24只自发性高血压大鼠(SHR)随机分为模型组和电针组各12只。电针组大鼠采用毫针分别于"百会"和双侧"太冲"直刺1~2 mm,进针后不施任何补泻手法。"百会"与右侧"太冲"分别连接韩氏电针仪的正负极,留针20 min。于每天上午针刺1次,连续针刺30天。正常组和模型组每天置于与电针组相同的固定装置中保持20 min。各组于开始针刺前1天及针刺第6、12、18、24、30天测量收缩压。以超声心动检测大鼠左心室肥厚程度和功能[包括舒张末左室后壁厚度(LVP-WT)、舒张末室间隔厚度(IVST)、左室舒张末内径(LVEDD)和左室射血分数(LVEF)],左心室质量指数(LVMI),HE染色观察心肌组织形态,并通过RT-PCR和Western blot技术检测各组大鼠心肌组织中磷脂酰肌醇激酶(PI3K)、蛋白激酶B (Akt)、哺乳动物雷帕霉素靶蛋白(m TOR)、同源性磷酸酶-张力蛋白(PTEN)、心房钠尿肽(ANP)蛋白与mRNA表达。结果与正常组比较,模型组大鼠LVMI、LVP-WT、IVST显著升高,LVEDD、LVEF显著降低(P <0. 01)。与模型组比较,电针组LVMI、LVP-WT、IVST明显降低,LVEDD、LVEF显著升高(P <0. 05或P <0. 01)。与正常组比较,模型组的心肌细胞排列相对紊乱,细胞横截面积明显变大,细胞间距变宽,细胞核增大深染。与模型组比较,电针组单位视野内细胞核的数量增多,心肌细胞横截面积相对较小,细胞间距相对更窄。与正常组比较,模型组心肌组织PI3K、Akt、m TOR蛋白和mRNA表达显著降低,PTEN蛋白和mRNA表达升高(P <0. 05或P <0. 01)。与模型组比较,电针组心肌组织PI3K、Akt、m TOR蛋白和mRNA表达显著升高,PTEN蛋白和mRNA表达降低(P <0. 05或P <0. 01)。结论电针"百会""太冲"可有效改善SHR心肌肥厚,电针激活PI3K/Akt通路可能是其机制之一。

Objective To investigate the effects of electroacupuncture( EA) on myocardial hypertrophy in spontaneously hypertensive rats( SHRs). Methods A total of 12 male 12-week-old Wistar Kyoto rats( WKY) were selected as normal control group,and 24 SHRs were randomized into model and EA group,with 12 in each group. EA was applied on bilateral'Taichong'( LR3) and'Baihui'( DU20) of SHRs in EA group,direct inserting 1 ~ 2 mm,without any reinforcing-reducing methods. 'Baihui'( DU20) and right side 'Taichong'( LR3) were respectively connected to the positive and negative poles of the HAN’s electro-acupuncture instrument,and the needle was retained for 20 minutes. EA was performed once a day for 30 days. The normal control group and the model group were placed in the same fixture as the EA group for 20 min each day. Systolic blood pressure was measured one day before the start of acupuncture and on the 6 th,12 th,18 th,24 th,and 30 th day of the acupuncture. Echocardiographic was used to detect the left ventricular hypertrophy and function including left ventricular posterior wall thickness( LVP-WT),interventricular septum thickness( IVST),left ventricular end-diastolic diameter( LVEDD),and left ventricular ejection fraction( LVEF),and left ventricular mass index( LVMI). The myocardial morphology was observed by HE staining,and phosphatidylinositol kinase( PI3 K),protein kinase B( Akt),mammalian rapamycin target of rapamycin( m TOR),homologous phosphatase tensin( PTEN),atrial natriuretic peptide( ANP) protein and mRNA expression in myocardial tissue of each group were detected by RT-PCR and Western blot. Results Compared with the normal control group,LVMI,LVP-WT and IVST in the model group were significantly increased,LVEDD and LVEF significantly decreased( P < 0. 01). Compared with the model group,LVMI,LVP-WT,and IVST of EA group were significantly decreased,LVEDD and LVEF significantly increased( P < 0. 05 or P < 0. 01). Compared with the normal control group,the myocardial cells in the model group were relatively disordered,the cross-sectional area of the cells was significantly enlarged,the cell spacing was widened,and the nucleus was enlarged and deeply stained.Compared with the model group,the number of nuclei in the unit visual field of EA group increased,the cross-sectional area of the cardiomyocytes was relatively small,and the cell spacing was relatively narrow. Compared with the normal control group,the expression of PI3 K,Akt,m TOR protein and mRNA in the myocardial tissue of the model group was significantly decreased,and the expression of PTEN protein and mRNA was increased( P < 0. 05 or P <0. 01). Compared with the model group,the expression of PI3 K,Akt,m TOR protein and mRNA in the EA group was significantly increased,and the expression of PTEN protein and mRNA was decreased( P < 0. 05 or P < 0. 01).Conclusion EA at 'Baihui'( DU20) and 'Taichong'( LR3) could effectively improve cardiac hypertrophy of SHR,and activation of PI3 K/Akt pathway by EA may be one of its mechanisms.