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Title: [Electroacupuncture of acupoints of heart meridian ameliorates acute myocardial ischemia via Akt/mTOR pathway].
Author: Wu LB, Zhang F, Yu Q, Wang MJ, Jiang ZM, Zhao LN, Wang J, Cai RL, Wu ZJ, Hu L.
Journal: Zhen Ci Yan Jiu; 2022 Feb 25; 47(2):121-8. PubMed ID: 35218621.
Abstract:
OBJECTIVE: To observe the effect of electroacupuncture (EA) on the expression of myocardial protein kinase B (Akt) and mammalian target of rapamycin (mTOR) in acute myocardial ischemia (AMI) rats. METHODS: Thirty male SD rats were randomly divided into control, model and EA groups (n=10 in each group). The AMI model was established by occlusion of the descending anterior branch (DAB) of the left coronary artery. EA (2 Hz, 1-2 mA) was applied to bilateral "Shenmen" (HT7) and "Tongli" (HT5) for 20 min, once daily for consecutive 7 days. The electrocardiogram (ECG) of nape-xiphoid lead was recorded for assessing changes of myocardial ischemia. Histopathologic changes of the ischemic myocardial tissue were observed after H.E. staining and ultra-microstructural changes of cardiomyocytes observed by transmission electron microscopy (TEM). The expression levels of Akt, phosphorylated-Akt (p-Akt), mTOR and phosphorylated-mTOR (p-mTOR) in the myocardium were detected by Western blot, followed by calculating the ratios of p-Akt/Akt and p-mTOR/mTOR. RESULTS: Following ligature of DAB, the ECG-ST level was significantly increased in the model group in comparison with the control group (P<0.01). At 30 min after treatment, the ECG-ST level decreased significantly compared with the model group (P<0.01). At the end of the 7-day treatment period, the ECG-ST level increased compared with the model group (P<0.05). The levels of myocardial p-Akt and p-mTOR protein expression, and the ratios of p-Akt/Akt and p-mTOR/mTOR were significantly lower in the model group than those in the control group (P<0.01), and considerably increased in the EA group than in the model group (P<0.01). No significant differences were found among the three groups in the expression levels of Akt and mTOR proteins (P>0.05). Outcomes of H.E. staining and TEM showed damage of mitochondria and occurrence of a large number of autophagosomes in myocardiocytes in the model group, which was milder in the EA group. CONCLUSION: EA at HT5 and HT7 can improve AMI in AMI rats, which may be related to its effect in facilitating Akt/mTOR signaling. 目的：观察电针对急性心肌缺血(AMI)大鼠心肌组织自噬相关通路蛋白激酶B(Akt)/哺乳动物雷帕霉素靶蛋白(mTOR)的影响，探讨电针对AMI的治疗作用机制。方法：SD大鼠随机分为假手术组、模型组、电针组，每组10只。采用冠状动脉左旋前降支结扎法建立AMI模型。电针组电针“神门”“通里”，每次20 min，每日1次，共7 d。记录各组大鼠在造模前、造模后、治疗后30 min和7 d的心电图并分析ST段电位。治疗7 d后，取心尖左心室肌组织HE染色并观察局部组织病理变化；透射电镜观察心肌细胞超微结构改变；蛋白免疫印迹法检测心肌组织Akt、磷酸化Akt(p-Akt)、mTOR、磷酸化mTOR(p-mTOR)表达水平，并计算各组p-Akt/Akt、p-mTOR/mTOR比值。结果：造模后，模型组和电针组心电图ST段均较假手术组显著升高(P<0.01)；治疗后30 min，电针组心电图ST段较模型组显著下降(P<0.01)；治疗7 d后，电针组心电图ST段较模型组升高(P<0.05)。假手术组心尖区域心肌纤维排列整齐致密，结构完整，电镜观察显示线粒体结构完整，自噬小体较少；模型组心尖区域出现心肌纤维结构破坏、肌浆凝聚、心肌细胞肥大等病理改变，电镜观察显示线粒体损伤，自噬小体数量较多；电针组心尖区域组织病变程度较模型组减轻，电镜观察显示线粒体损伤程度较模型组减轻，自噬小体数量减少。3组大鼠心肌组织Akt、mTOR水平组间比较差异无统计学意义(P＞0.05)；模型组p-Akt、p-mTOR水平及p-Akt/Akt、p-mTOR/mTOR均较假手术组下降(P<0.01)；电针组p-Akt、p-mTOR水平及p-Akt/Akt、p-mTOR/mTOR均较模型组升高(P<0.01)。结论：电针大鼠“神门”“通里”可能通过激活AMI大鼠心肌细胞Akt/mTOR通路抑制过度自噬，从而发挥对AMI的治疗作用。.

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