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[针刺对高脂血症小鼠心脏的保护作用及其机制]

[Protective effect of acupuncture on heart in mice with hyperlipemia and its mechanism].

作者信息

Shen Hong-Bo, Zhang Li, Guo Jia, Ji Xiao-Lan, Peng Bo, Li Fu-Yun, Liu Cheng, Huo Ze-jun

出版信息

Zhongguo Zhen Jiu. 2014 Apr;34(4):373-8.

PMID:24946643
Abstract

OBJECTIVE

To observe the inhibiting effect of acupuncture on blood lipid, myocardial hypertrophy and fibrosis in mice with hyperlipemia, and explore its possible action mechanism.

METHODS

Ten inbred mice (C57) were applied. Forty ApoE(-/-) mice who removed gene of apolipoprotein E were randomly divided into a control group, a non-acupoint group, an acupoint group and a medication group. The points 0. 5 cm and 1 cm next to the end of mice tail were respectively punctured in the non-acupoint group; "Neiguan" (PC 6) and "Fenglong" (ST 40) were punctured in the acupoint group; intragastric administration of simvastatin was applied in the medication group. After 8 weeks of treatment, the changes of total cholesterol (TC) and ratio of heart to body mass in each group were measured; changes of cardiac muscle fiber and ventricular wall thickness were observed; enzyme linked immunosorbent assay (ELISA) was used to test the level of angiotensin II (Ang I ) in plasma, and western blotting method was used to test protein content of angiotensin II type 1 receptor (AT1R) and endothelin-1 type A receptor (ETAR) in the heart.

RESULTS

After 8 weeks of intervention, compared with the control group, rising range of blood lipid was obviously decreased (P<0.01) in the acupoint group and medication group, ratio of P<0.01), myocardial heart to body mass was decreased (P<0.05), thickness of ventricular wall was reduced (P fibrosis was relieved, levels of Ang II and ET-1 in plasma were decreased (P<0. 05), content of NO was increased (P<0. 05), and protein content of AT1R and ETAR was decreased in the heart (P<0. 05).

CONCLUSION

  1. could inhibit the rising of blood lipid in ApoE(-/-) mice, lower the levels of Ang II and ET-1 in peripheral blood, increase the content of NO and inhibit the expression of AT1R and ETAR in heart tissue, which could relieve myocardial hypertrophy and fibrosis to play a protective role on heart.
摘要

目的

观察针刺对高脂血症小鼠血脂、心肌肥厚及纤维化的抑制作用,并探讨其可能的作用机制。

方法

选用10只近交系小鼠(C57)。将40只敲除载脂蛋白E基因的ApoE(-/-)小鼠随机分为对照组、非穴位组、穴位组和药物组。非穴位组在小鼠尾尖旁0.5 cm和1 cm处分别针刺;穴位组针刺“内关”(PC 6)和“丰隆”(ST 40);药物组灌胃给予辛伐他汀。治疗8周后,测定各组总胆固醇(TC)及心体质量比的变化;观察心肌纤维及心室壁厚度的变化;采用酶联免疫吸附测定法(ELISA)检测血浆中血管紧张素Ⅱ(AngⅡ)水平,采用蛋白质印迹法检测心脏中血管紧张素Ⅱ1型受体(AT1R)和内皮素-1 A型受体(ETAR)的蛋白含量。

结果

干预8周后,与对照组比较,穴位组和药物组血脂升高幅度明显降低(P<0.01),心体质量比降低(P<0.05),心室壁厚度减小(P<0.01),心肌纤维化减轻,血浆中AngⅡ和ET-1水平降低(P<0.05),一氧化氮(NO)含量增加(P<0.05),心脏中AT1R和ETAR蛋白含量降低(P<0.05)。

结论

针刺“内关”(PC 6)、“丰隆”(ST 40)可抑制ApoE(-/-)小鼠血脂升高,降低外周血中AngⅡ和ET-1水平,增加NO含量,抑制心脏组织中AT1R和ETAR的表达,从而减轻心肌肥厚和纤维化,对心脏起到保护作用。

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