Effect of Astragaloside IV on Cardiac Function of Rats with Complex Harmful Fluid Retention

CHEN Qian; JI Xu-ming; KAN Dong-fang; HAN Xiao-chun; WANG Yuan; YU Wan-chen; WANG Shi-jun

doi:10.13422/j.cnki.syfjx.2017140100

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Effect of Astragaloside IV on Cardiac Function of Rats with Complex Harmful Fluid Retention

更新时间：2024-01-04

- Effect of Astragaloside IV on Cardiac Function of Rats with Complex Harmful Fluid Retention
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 23, Issue 14, Pages: 100-105(2017)
- 作者机构：
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- DOI：10.13422/j.cnki.syfjx.2017140100
  CLC： R285.5
- Published：2017
- 稿件说明：
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CHEN Qian, JI Xu-ming, KAN Dong-fang, et al. Effect of Astragaloside IV on Cardiac Function of Rats with Complex Harmful Fluid Retention[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(14): 100-105.
DOI：

CHEN Qian, JI Xu-ming, KAN Dong-fang, et al. Effect of Astragaloside IV on Cardiac Function of Rats with Complex Harmful Fluid Retention[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(14): 100-105. DOI： 10.13422/j.cnki.syfjx.2017140100.

摘要

目的：探讨黄芪甲苷对水饮内停大鼠心脏功能的改善作用。方法：SD大鼠采用肩胛区皮下注射异丙肾上腺素（ISO）加气管置管复合干预因素建立上焦水饮内停大鼠模型，建模成功后随机分为模型组、黄芪甲苷低、中、高剂量组及阳性药组（芪苈强心胶囊），另设立正常组作为对照，每组10只大鼠。分别给予等体积羧甲基纤维素钠（0.5%），黄芪甲苷（20，40，80 mg·kg-1·d-1），芪苈强心胶囊（1 g·kg-1·d-1）灌胃，持续给药2周，通过大鼠体重（BW），心重指数（HWI），左心室质量指数（LVWI）观察心肌肥厚程度；苏木素-伊红（HE）染色法和胶原容积分数（CVF）观察心脏组织形态学改变；大鼠超声心动图检测左心室射血分数（LVEF）及左心室短轴缩短分数（LVFS）改变；酶联免疫吸附测定（ELISA）检测血浆肌酸激酶（CK）的表达水平。结果：与正常组比较，模型组大鼠BW显著降低（P<0.01），HWI和LVWI显著增高（P<0.01），心肌肥厚较为明显，LVEF，LVFS显著降低（P<0.01），心肌CVF及血浆CK明显增高（P<0.05，P<0.01），心肌病理损伤较为明显；给药干预后，黄芪甲苷（40，80 mg·kg-1·d-1）剂量组大鼠BW明显增高（P<0.05），HWI，LVWI明显升高降低（P<0.05，P<0.01），可以有效缓解心肌肥厚，且升高模型大鼠的LVEF及LVFS（P<0.05），改善心脏功能，模型大鼠的CK，CVF明显降低（P<0.05），减轻心肌病理损伤。结论：黄芪甲苷可以通过抑制上焦水饮内停大鼠心肌纤维化、降低左室厚度、改善血流动力学等方面发挥保护心脏的作用。

Abstract

Objective: To investigate the effect of astragaloside Ⅳ on improving the cardiac function of the rats with complex harmful fluid retention. Method: Subcutaneous injection of isoproterenol (ISO) in the scapularis region and tracheal intubation were used to establish the rat models of harmful fluid retention in upper warmer. After successful modeling

the rats were randomly divided into model group

astragalaside Ⅳ low

middle and high-dose groups

positive control group (Qili Qiangxin capsules) and normal group

n=10 in each group. The rats in the astragalaside Ⅳ groups were treated with astragalaside Ⅳ at doses of 20

80 mg·kg-1·d-1 as low

middle and high dose groups respectively; the rats in model group and positive control group were treated with 0.5% CMC-Na solution and Qiliqiangxin capsule (1 g·kg-1·d-1) with equal volume. After treatment for 2 weeks

the degree of myocardial hypertrophy was observed by the body weight (BW)

heart weight index (HWI) and left ventricular weight index (LVWI); hematoxylin eosin (HE) staining and collagen volume fraction (CVF) were used to observe the changes of cardiac pathology; left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were measured by echocardiography; and enzyme linked immunosorbent assay (ELISA) was used to detect the level of plasma creatine kinase (CK). Result: As compared with the normal group

the level of BW was significantly lower (P<0.01); HWI and LVWI were significantly higher (P<0.01)

with more obvious myocardial hypertrophy; LVEF and LVFS were significantly reduced (P<0.01); and myocardial CVF and plasma CK was significantly increased (P<0.05

P<0.01) in model group

with more obvious myocardial pathological injury. After treatment

the level of BW was significantly higher ( P<0.05) and the HWI

LVWI were decreased in the astragalaside Ⅳ 40

80 mg·kg-1·d-1 dose groups as compared with the model group (P<0.05

P<0.01). This can effectively alleviate myocardial hypertrophy. Moreover

the high-dose and middle-dose astragalaside Ⅳ groups significantly increased LVEF and LVFS to improve cardiac function

reduced CK

CVF(P<0.05)

and relieved myocardial pathological damages. Conclusion: Astragalaside Ⅳ can protect the heart by inhibiting the myocardial fibrosis

reducing left ventricular thickness and improving hemodynamics in the rat models of harmful fluid retention in upper warmer.

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