Wu Sheng-Bing, Cao Jian, Gao Fang, Wang Li-Na, Chang Meng-Juan, Xue Jing-Jing, Zhang Tian-Ning, Zhou Mei-Qi
Zhen Ci Yan Jiu. 2013 Apr;38(2):87-92.
To observe the effect of electroacupuncture (EA) on the expression of myocardial 1-phosphatidylinositol 3-kinase (PI 3 K), hypoxia-inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) in rats with cerebral-cardiac syndrome (CCS), so as to reveal its mechanism underlying reducing ischemic myocardial injury.
Forty SD rats were randomly and equally divided into sham-operation, model, EA and non-acupoint (the lateral-superior side of the hip) groups (10 rats/group). CCS model was established by injection of collagenase (1 U/microL) and heparin (7 U/microL) into the right caudate nucleus. Following modeling, EA (1.5 mA, 2 Hz, 20 min) was applied to "Shuigou" (GV 26), "Fengfu" (GV 16), "Neiguan" (PC 6) and "Xinshu" (BL 15) acupoints, once daily for three consecutive days. The expression levels of PI 3 K,HIF-1alpha and VEGF in the myocardium were detected by immunohistochemistry.
Compared with the sham-operation group, the expression levels of myocardial PI 3 K, HIF-1a and VEGF proteins were significantly increased in the model group (P<0.01). While in comparison with the model group, there were little increase in the non-acupoint group (P>0.05) and considerable increase in the expression levels of the 3 myocardial proteins in the EA group (P<0.05).
EA intervention has a function in upregulating the expression of myocardial VEGF, HIF-1alpha and PI 3 K proteins in CCS rats, which maybe contribute to its protective effect on ischaemic myocardial injury.
观察电针(EA)对脑心综合征(CCS)大鼠心肌1-磷脂酰肌醇3激酶(PI 3 K)、缺氧诱导因子-1α(HIF-1α)和血管内皮生长因子(VEGF)表达的影响,以揭示其减轻缺血性心肌损伤的机制。
40只SD大鼠随机等分为假手术组、模型组、电针组和非穴位组(每组10只)。通过向右侧尾状核注射胶原酶(1 U/μL)和肝素(7 U/μL)建立CCS模型。造模后,将电针(1.5 mA,2 Hz,20分钟)应用于“水沟”(GV 26)、“风府”(GV 16)、“内关”(PC 6)和“心俞”(BL 15)穴位,每天1次,连续3天。采用免疫组织化学法检测心肌中PI 3 K、HIF-1α和VEGF的表达水平。
与假手术组比较,模型组心肌PI 3 K、HIF-1α和VEGF蛋白表达水平显著升高(P<0.01)。与模型组比较,非穴位组上述心肌蛋白表达水平升高不明显(P>0.05),电针组心肌PI 3 K、HIF-1α和VEGF蛋白表达水平显著升高(P<0.05)。
电针干预可上调CCS大鼠心肌VEGF、HIF-1α和PI 3 K蛋白的表达,这可能是其对缺血性心肌损伤具有保护作用的机制之一。