针刺对自发性高血压大鼠心肌ANP、ACE2表达和Ang（1-7）/Ang■ 比值的影响

摘要
图/表
参考文献(20)
相关文章 (15)

全文: PDF (947 KB) HTML (1 KB)
输出: BibTeX | EndNote (RIS)

摘要目的通过观察自发性高血压大鼠（SHR）心肌组织结构和肾素-血管紧张素-醛固酮系统（RAS）作用因子表达的变化，探究针刺对高血压心肌肥厚的防护机制。方法将10只WKY大鼠作为空白组，将20只SHR按照随机数字表法分为模型组和针刺组，每组各10只。所有大鼠均为10周龄SPF级雄性大鼠。适应性饲养1周后，针刺组大鼠用毫针于“百会”和双“太冲”直刺，每天1次，连续干预28 d。模型组和空白组不做针刺干预。于实验第1、7、14、21、28天针刺前测量血压值。实验结束后称取大鼠全心及左心室重量，并计算心脏重量指数（HWI）和左心室重量指数（LVWI）。应用HE和Masson染色法观察心肌组织形态，并通过Real-tiem PCR、Western blot、酶联免疫吸附测定（ELISA）等技术检测各组大鼠心肌组织中心房钠尿肽（ANP）、血管紧张素转换酶2（ACE2）、血管紧张素1-7[Ang（1-7）]和AngⅡ的表达，并计算Ang（1-7）/AngⅡ。结果与空白组比较，模型组大鼠收缩压（SBP）、HWI、LVWI显著升高（P ＜ 0.01）。与模型组比较，针刺组大鼠SBP、HWI、LVWI值明显降低（P ＜ 0.05或P ＜ 0.01）。病理切片结果显示，与空白组比较，模型组大鼠心肌细胞的细胞体积明显变大，且排列相对紊乱，同时细胞间距变宽，充斥着大量被蓝染的纤维。与模型组比较，针刺组大鼠心肌细胞体积更小，细胞间距更窄，细胞间隙蓝染的纤维变少。与空白组比较，模型组心肌组织的ACE2的表达水平和Ang（1-7）/AngⅡ显著降低（P ＜ 0.01），ANP的表达水平升高（P ＜ 0.01）。与模型组比较，针刺组ACE2的表达水平和Ang（1-7）/AngⅡ的比值显著升高（P ＜ 0.01），ANP的表达水平降低（P ＜ 0.01）。结论针刺“百会”“太冲”可通过调节ACE2/Ang（1-7）的表达，有效降低SHR血压，并减轻其心肌肥厚的程度。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章
	纪智袁静云王紫娟张跃梁靖蓉吴娇娟刘清国

关键词 ：高血压, 针刺, 心肌肥厚, 血管紧张素转换酶2, 血管紧张素1-7

Abstract：Objective To investigate the protective mechanism of acupuncture on myocardial hypertrophy by observing the changes of myocardial tissue structure and renin angiotension system (RAS) system action factor expression in spontaneously hypertensive rats (SHR). Methods Ten Wistar Kyoto rats (WKY) were selected as normal control group, 20 SHRs were divided into model group and acupuncture group by random number table method, with 10 rats in each group. All rats were SPF grade male 10-week-old rats. After one week of acclimatization, acupuncture was applied on Taichong (LR3) and Baihui (DU20) of SHRs in acupuncture group once a day for 28 days. The other two groups only received the same grasping and fixation stimulation. Blood pressure was measured before acupuncture on day 1, 7, 14, 21 and 28. At the end of the experiment, the weight of the whole heart and left ventricle of the rats were weighed, and ratio of left ventricle weight to body weight (LVWI), heart weight index (HWI) were calculated. HE and Masson staining method were applied to observe the myocardial tissue morphology, and Real-time RCR, Western blot, enzyme linked immunosorbent assay (ELISA) were used to detect the expression of atrial natriuretic peptide (ANP), angiotensin-converting enzyme 2 (ACE2), angiotensin (1-7) [Ang(1-7)], AngⅡ and Ang(1-7)/AngⅡ, as well as the underlying mechanisms were investigated. Results Compared with normal control group, the systolic blood pressure (SBP), HWI and LVWI in the model group were significantly increased (P ＜ 0.01). Compared with the model group, SBP, HWI and LVWI values in the acupuncture group were significantly decreased (P ＜ 0.05 or P ＜ 0.01). The pathological results showed that compared with normal control group, the cell volume of rat cardiac muscle cells in the model group was significantly larger, and the arrangement was relatively disordered. Meanwhile, the cell spacing was widened, and there were a lot of blue-stained fibers. Compared with the model group, the cardiac muscle cells in the acupuncture group were smaller in volume, narrower in cell spacing, and fewer blue-stained fibers in the cell space. Compared with normal control group, the expression level of ACE2 and Ang (1-7)/AngⅡ of myocardial tissue in model group significantly decreased (P ＜ 0.01), the expression level of ANP significantly increased (P ＜ 0.01). Compared with model group, the expression level of ACE2 and Ang (1-7)/AngⅡ in acupuncture group significantly increased (P ＜ 0.01), the expression level of ANP significantly decreased (P ＜ 0.01). Conclusion Acupuncture at LR3 and DU20 could reduce blood pressure and inhibit the development of cardiac hypertrophy, which might be mediated by the regulation of ACE2/Ang(1-7) pathway.

Key words： Hypertension Acupuncture Myocardial hypertrophy Angiotensin-converting enzyme 2 Angiotensin (1-7)

基金资助:国家自然科学基金资助项目（81373727、815740 69、81774413）；
北京市自然科学基金资助项目（7162121）。

通讯作者: 刘清国（1963-），男，教授，针灸学博士，博士研究生导师；研究方向：针灸临床与机制研究。

引用本文:

纪智袁静云王紫娟张跃梁靖蓉吴娇娟刘清国. 针刺对自发性高血压大鼠心肌ANP、ACE2表达和Ang（1-7）/Ang■ 比值的影响[J]. 中国医药导报, 2019, 16(17): 4-8.
JI Zhi YUAN Jingyun WANG Zijuan ZHANG Yue LIANG Jingrong WU Jiaojuan LIU Qingguo. Effect of acupuncture on the expression of ANP, ACE2 and Ang(1-7)/ AngⅡ ratio in heart tissue of spontaneously hypertensive rats. 中国医药导报, 2019, 16(17): 4-8.

链接本文:

http://www.yiyaodaobao.com.cn/CN/ 或 http://www.yiyaodaobao.com.cn/CN/Y2019/V16/I17/4

[1] 吴小龙，薛明明，司明明，等.心肌肥厚发生机制及药物治疗的研究进展[J].医学综述，2015，21（5）：803-806.
[2] Draper TS，Silver JS，Gaasch WH. Adverse Structural Remodeling of the Left Ventricle and Ventricular Arrhythmias in Patients With Depressed Ejection Fraction [J]. J Card Fail，2015，21（2）：97-102.
[3] 陆启璇.血管紧张素转换酶2-Ang（1-7）-Mas轴对心血管系统保护作用研究进展[J].长治医学院学报，2018，32（1）：77-80.
[4] Xin JJ，Gao JH，Wang YY，et al. Antihypertensive and Antihypertrophic Effects of Acupuncture at PC6 Acupoints in Spontaneously Hypertensive Rats and the Underlying Mechanisms [J]. Evid Based Complement Alternat Med，2017，2017：9708094. doi：10.1155/2017/9708094.
[5] 李佳，吴松，唐宏图，等.电针内关穴对心肌肥厚大鼠Raf、ERK1/2及p-ERK1/2表达的影响[J].中国中西医结合杂志，2016，36（11）：1335-1339.
[6] 余曙光，徐斌.实验针灸学[M].北京：人民卫生出版社，2012：269-270.
[7] Nadruz W，Shah AM，Solomon SD. Diastolic Dysfunction and Hypertension [J]. Med Clin North Am，2017，101（1）：7-17.
[8] 范金茹，王行宽，熊国强.高血压左室肥厚中医病名、病位、病因病机探讨[J].中医药通报，2005，4（2）：19-21.
[9] 吕仕超，杨锡燕，张军平.中医药治疗高血压心肌纤维化的研究[J].世界科学技术-中医药现代化，2015，17（6）：1295-1299.
[10] Jia W，Zhang Y，Sui M，et al. Effect of acupuncture on the genetic expression of myocardial endothelin-1 and atrial natriuretic peptide in Rats with stress-induced prehypertension [J]. J Tradit Chin Med，2017，4（1）：82-91.
[11] Huo ZJ，Li Q，Tian GH，et al. The ameliorating effects of long-term electroacupuncture on cardiovascular remodeling in spontaneously hypertensive rats [J]. BMC Complement Altern Med，2014，14：118. doi：10.1186/1472-6882-14-118.
[12] Li X，Lan Y，Wang Y，et al. Telmisartan suppresses cardiac hypertrophy by inhibiting cardiomyocyte apoptosis via the NFAT/ANP/BNP signaling pathway [J]. Mol Med Rep，2017，15（5）：2574-2582.
[13] 王阿慧，孙晓鸥，刘青，等.西地那非对主动脉弓缩窄诱导大鼠心肌肥大的保护作用[J].广东药学院学报，2016， 32（4）：475-480.
[14] 杨俊，徐如祥.心房钠尿肽生理、生化及其临床意义[J].南方医科大学学报，2000，20（4）：373-374.
[15] Patel VB，Zhong JC，Grant MB，et al. Role of the ACE2/Angiotensin 1-7 Axis of the Renin-Angiotensin System in Heart Failure [J]. Circ Res，2016，118（8）：1313-1326.
[16] Zhong J，Basu R，Guo D，et al. Angiotensin-converting enzyme 2 suppresses pathological hypertrophy，myocardial fibrosis，and cardiac dysfunction [J]. Circulation，2010， 122（7）：717-728.
[17] Wang J，He W，Guo L，et al. The ACE2-Ang（1-7）-Mas receptor axis attenuates cardiac remodeling and fibrosis in post-myocardial infarction [J]. Mol Med Rep，2017，16（2）：1973-1981.
[18] 钟久昌，朱鼎良.血管紧张素转换酶2与高血压[J].高血压杂志，2005，13（11）：682-686.
[19] Pereira RM，Dos Santos RA，Teixeira MM，et al. The renin-angiotensin system in a rat model of hepatic fibrosis：evidence for a protective role of Angiotensin-（1-7）[J]. J Hepatol，2007，46（4）：674-681.
[20] Grobe JL，Mecca AP，Lingis M，et al. Prevention of angiotensin Ⅱ-induced cardiac remodeling by angiotensin-（1-7）[J]. Am J Physiol Heart Circ Physiol，2007，292（2）：H736-H742.