Kong Su-Ping, Zhang Xin, Tan Qi-Wen
Department of Acupuncture and Moxibustion, Affiliated Hospital of Shandong University of TCM, Jinan 250011, China.
Zhongguo Zhen Jiu. 2013 Jun;33(6):529-32.
To explore the protective mechanism of acupuncture on myocardial ischemia-reperfusion injury.
Fifty Wistar rats were randomly divided into a sham-operation group, a model group, a Jiaji group , a Neiguan group and a Yanglingquan group, 10 rats in each group. The model of myocardial ischemia-reperfusion injury was duplicated by ligating the left anterior descending coronary artery (LADCA) in the later four groups, and the LADCA was not ligated in the sham-operation group. The rats in the treatment groups were treated with electroacupuncture at "Jiaji" (EX-B 2), "Neiguan" (PC 6) and "Yanglingquan" (GB 34) on both sides, respectively, once a day for 7 days. No interventions were produced in the sham-operation group and model group. Myocardial apoptosis were examined by the TUNEL method. The expressions of Bcl-2 and Bax proteins were measured by immunohistochemical method.
Apoptosis index(AI) was significantly lower in the Jiaji group, Neiguan group and sham-operation group compared with model group (P < 0.01). Compared with the sham-operation group, AI were significantly increased in other groups (all P < 0.01). There was no significant difference in AI between Jiaji and Neiguan group (P > 0.05). Compared with the model group, the expression of Bcl-2 was significantly increased and Bax protein was significantly decreased in Jiaji group and Neiguan group (both P < 0.01). The expressions of Bcl-2 and Bax proteins were significantly increased in other groups compared with the sham-operation group (all P < 0.01). There was no significant difference in the expression of Bcl-2 and Bax proteins between Jiaji and Neiguan group (P > 0.05).
Electroacupuncture at both Jiaji (EX-B 2) and Neiguan (PC 6) has protective effects on myocardial ischemia-reperfusion injury, and the mechanism is closely related to inhibiting myocardial apoptosis by adjusting the expression of Bcl-2 and Bax.
探讨针刺对心肌缺血再灌注损伤的保护机制。
将50只Wistar大鼠随机分为假手术组、模型组、夹脊组、内关组和阳陵泉组,每组10只。后四组采用结扎左冠状动脉前降支(LADCA)的方法复制心肌缺血再灌注损伤模型,假手术组不结扎LADCA。治疗组大鼠分别双侧电针“夹脊”(EX-B 2)、“内关”(PC 6)和“阳陵泉”(GB 34),每日1次,连续7天。假手术组和模型组不做干预。采用TUNEL法检测心肌细胞凋亡情况。采用免疫组织化学法检测Bcl-2和Bax蛋白的表达。
夹脊组、内关组和假手术组凋亡指数(AI)明显低于模型组(P < 0.01)。与假手术组比较,其他组AI均明显升高(均P < 0.01)。夹脊组与内关组AI比较差异无统计学意义(P > 0.05)。与模型组比较,夹脊组和内关组Bcl-2表达明显升高,Bax蛋白明显降低(均P < 0.01)。与假手术组比较,其他组Bcl-2和Bax蛋白表达均明显升高(均P < 0.01)。夹脊组与内关组Bcl-2和Bax蛋白表达比较差异无统计学意义(P > 0.05)。
夹脊(EX-B 2)和内关(PC 6)电针均对心肌缺血再灌注损伤具有保护作用,其机制可能与调节Bcl-2和Bax表达抑制心肌细胞凋亡密切相关。