芪苈强心胶囊对压力超负荷心力衰竭大鼠内皮损伤及能量代谢的影响

张军芳; 唐思文; 王宏涛; 徐登峰; 贾振华; 魏聪; 吴以岭

doi:10.13288/j.11-2166/r.2013.14.022

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芪苈强心胶囊对压力超负荷心力衰竭大鼠内皮损伤及能量代谢的影响

实验研究 | 更新时间：2021-11-17

- 芪苈强心胶囊对压力超负荷心力衰竭大鼠内皮损伤及能量代谢的影响
- Effect of Qili Heart-Strengthening Capsule on Endothelial Injury and Energy Metabolism in Rats with Pressure Overload Heart Failure
- 中医杂志 2013年54卷第14期页码：1221-1224
- 作者机构：
  
  1. 河北医科大学中西医结合教研室
  2. 河北省络病重点实验室
  3. 国家中医药管理局心脑血管络病重点研究室
  4. 河北以岭医药研究院
  5. 河北医科大学附属以岭医院
- 作者简介：
- 基金信息：
  
  国家重点基础研究发展计划（“973”计划）资助项目（2012CB518606）
- DOI：10.13288/j.11-2166/r.2013.14.022
  中图分类号： R285.5
- 纸质出版：2013
- 稿件说明：
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[1]张军芳,唐思文,王宏涛,徐登峰,贾振华,魏聪,吴以岭.芪苈强心胶囊对压力超负荷心力衰竭大鼠内皮损伤及能量代谢的影响[J].中医杂志,2013,54(14):1221-1224+1229.

ZHANG Junfang1, TANG Siwen2, 3, et al. Effect of Qili Heart-Strengthening Capsule on Endothelial Injury and Energy Metabolism in Rats with Pressure Overload Heart Failure[J]. Journal of Traditional Chinese Medicine2013, 54(14): 1221-1224.
[1]张军芳,唐思文,王宏涛,徐登峰,贾振华,魏聪,吴以岭.芪苈强心胶囊对压力超负荷心力衰竭大鼠内皮损伤及能量代谢的影响[J].中医杂志,2013,54(14):1221-1224+1229. DOI： 10.13288/j.11-2166/r.2013.14.022.

ZHANG Junfang1, TANG Siwen2, 3, et al. Effect of Qili Heart-Strengthening Capsule on Endothelial Injury and Energy Metabolism in Rats with Pressure Overload Heart Failure[J]. Journal of Traditional Chinese Medicine2013, 54(14): 1221-1224. DOI： 10.13288/j.11-2166/r.2013.14.022.

摘要

目的探讨芪苈强心胶囊治疗压力超负荷心力衰竭的可能机制。方法随机取SD大鼠15只为假手术组

采用升主动脉缩窄术建立压力超负荷心力衰竭大鼠模型

75只造模成功大鼠随机分为模型组、卡托普利组和芪苈强心高、中、低剂量组各15只。卡托普利组给予卡托普利片6.25mg/（kg·d）

芪苈强心高、中、低剂量组分别给予芪苈强心胶囊1.0、0.5、0.25g/（kg·d）

假手术组和模型组灌服等体积的0.5%羧甲基纤维素钠

各组连续灌胃6周。透射电镜观察心肌组织毛细血管超微结构

比较各组大鼠心肌组织三磷酸腺苷（ATP）、二磷酸腺苷（ADP）、一磷酸腺苷（AMP）含量

血管黏附因子1（ICAM-1）与内皮型一氧化氮合酶（eNOS）mRNA表达水平

AMP激活的蛋白激酶（AMPK）及其磷酸化AMPK（p-AMPK）蛋白表达。结果芪苈强心低、中剂量组及卡托普利组均显著增加心肌组织中ATP含量（P<0.01）

各给药组ADP明显升高（P<0.01）;芪苈强心高剂量组与卡托普利组ICAM-1mRNA表达降低、eNOSmRNA升高（P<0.05或P<0.01）;芪苈强心低、中、高剂量组与卡托普利组p-AMPK蛋白表达均显著升高（P<0.05或P<0.01）;各组大鼠心肌组织AMPK蛋白表达量差异无统计学意义（P>0.05）。结论芪苈强心具有保护压力超负荷大鼠心肌毛细血管内皮的作用

同时提高心脏能量负荷水平、改善能量代谢

其作用机制可能与激活AMPK-eNOS通路有关。

Abstract

Objective To study the effect and possible mechanism of Qili Heart-Strengthening Capsule [heart-strengthening capsule of Huangqi （Radix Astragali） and Tinglizi （Semen Lepidii）] on pressure overload heart failure. Methods Fifteen SD rats were randomly selected as the sham operation group. The ascending aorta constriction was conducted to establish the pressure overload heart failure models. Totally 75 successfully modeling rats were randomized into the model group

captopril group

Qili Heart-Strengthening Capsule high-dose

middle-dose and low-dose groups

with 15 in each. The captopril group was given 6.25 mg/（kg·d） captopril tablet. The Qili Heart-Strengthening Capsule high-dose

middle-dose and low-dose groups were given 1.0

0.5 and 0.25 g/（kg·d） Qili Heart-Strengthening Capsule respectively. The sham operation group and model group were given an equal volume of 0.5% sodium carboxymethyl cellulose. The administration lasted for 6 weeks. The ultrastructure of myocardial tissue capillaries was observed by transmission electron microscopy. The adenosine triphosphate （ATP）

adenosine diphosphate （ADP）

adenosine monophosphate （AMP）

intercellular adhesion molecule-1 （ICAM-1）

endothelial nitric oxide synthase （eNOS） mRNA expression

AMP-activated protein kinase （AMPK） and phosphorylated AMPK （p-AMPK） protein in the myocardial tissue was compared. Results The ATP contents in the Qili Heart-Strengthening Capsule middle-dose and low-dose groups and captopril group were significantly increased （P<0.01）. The ADP contents in all medication groups were significantly increased （P<0.01）. The ICAM-1mRNA expression was significantly decreased but the eNOS mRNA expression was significantly increased in the Qili Heart-Strengthening Capsule high-dose group and captopril group （P<0.05 or P<0.01）. The p-AMPK expression was significantly increased in the Qili Heart-Strengthening Capsule groups and captopril group （P<0.05 or P<0.01）. There was no significant difference between before and after treatment in the AMPK expression in all groups （P>0.05）. Conclusion Qili Heart-Strengthening Capsule can protect the myocardial capillary endothelial

increase the cardiac energy load level

improve the energy metabolism

and its mechanism may be related to the activation of AMPK-eNOS pathway.

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