Effect and Mechanism of Dendrobii Officinalis Caulis in Intervening and Preventing Myocardial Fibrosis in Rats with Heart Failure and Heart Qi Deficiency Syndrome After Ischemia-reperfusion

Qing-min LI; Wu-lin QU; Bo-jun CHEN

doi:10.13422/j.cnki.syfjx.20191502

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Effect and Mechanism of Dendrobii Officinalis Caulis in Intervening and Preventing Myocardial Fibrosis in Rats with Heart Failure and Heart Qi Deficiency Syndrome After Ischemia-reperfusion

Pharmacology | 更新时间：2021-02-09

- Effect and Mechanism of Dendrobii Officinalis Caulis in Intervening and Preventing Myocardial Fibrosis in Rats with Heart Failure and Heart Qi Deficiency Syndrome After Ischemia-reperfusion
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 25, Issue 15, Pages: 83-88(2019)
- 作者机构：
  
  1.广州中医药大学，广州　 510006；
  2.郴州市第一人民医院，湖南　郴州　 423000
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20191502
  CLC： R2-0; R22; R285.5
- Received：26 December 2018，
  
  Published Online：18 April 2019，
  
  Published：05 August 2019
- 稿件说明：
移动端阅览
Qing-min LI, Wu-lin QU, Bo-jun CHEN. Effect and Mechanism of Dendrobii Officinalis Caulis in Intervening and Preventing Myocardial Fibrosis in Rats with Heart Failure and Heart Qi Deficiency Syndrome After Ischemia-reperfusion[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(15): 83-88.
DOI：

Qing-min LI, Wu-lin QU, Bo-jun CHEN. Effect and Mechanism of Dendrobii Officinalis Caulis in Intervening and Preventing Myocardial Fibrosis in Rats with Heart Failure and Heart Qi Deficiency Syndrome After Ischemia-reperfusion[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(15): 83-88. DOI： 10.13422/j.cnki.syfjx.20191502.

摘要

目的：

基于缺血再灌注后心衰心气虚型大鼠模型心动周期、心肌病理切片、心肌半乳糖凝集素3(Gal-3)转化生长因子-

(TGF-

)，Smad同源物3重组蛋白(Smad3)蛋白表达情况，探讨铁皮石斛对模型大鼠心肌纤维化的干预效果。

方法：

采用冠状动脉左前降支进行结扎术建立心衰心气虚型大鼠模型，将大鼠分为正常组，模型组，缬沙坦组(9.43 mg·kg

－1

)，铁皮石斛组(10 mg·kg

－1

)共4组，每组10只，正常组和模型组给予等体积生理盐水。通过动物高分辨超声仪记录各组大鼠心动周期左室舒张末期内径(LVEDD)，左室收缩末期内径(LVESD)，左心射血分数(LVEF)，左心室短轴缩短率(LVFS)变化；酶联免疫吸附测定(ELISA)试剂盒测定I型胶原羧基端前肽(PICP)，Ⅲ型胶原羧基端前肽(PⅢNP)；苏木素-伊红(HE)染色观察心肌细胞形态变化，马松(Masson)染色观察心肌纤维组织、胶原组织变化，蛋白免疫印迹法(Western blot)检测4组小鼠心肌半乳糖凝集素3(Gal-3)，转化生长因子-

(TGF-

)，Smad同源物3重组蛋白(Smad3)蛋白表达情况。

结果：

与正常组比较，模型组LVEDD，LVEF，LVFS水平明显降低(

0.05)，LVESD，PICP，PIIINP水平升高(

0.05)，Gal-3，TGF-

，Smad3蛋白表达水平显著升高(

0.01)；与模型组比较，缬沙坦组、铁皮石斛组LVEDD，LVEF，LVFS明显升高(

0.05)，LVESD，PICP，PIIINP水平明显降低(

0.05)，Gal-3，TGF-

，Smad3蛋白表达水平明显降低(

0.05，

0.01)，且铁皮石斛组低于缬沙坦组(

0.05)；HE染色结果显示，铁皮石斛组心肌细胞形态明显改善，Masson染色结果显示，铁皮石斛组心肌纤维组织、胶原组织形态明显改善。

结论：

铁皮石斛可有效抑制缺血再灌注后心衰心气虚症候大鼠心肌纤维化，机制可能为降低Gal-3，TGF-

，Smad3蛋白表达有关。

Abstract

Objective:

To investigate the expressions of cardiac cycle

myocardial pathology

galectin-3 (Gal-3)

transforming growth factor-

(TGF-

)

Smad homologue 3 recombinant protein (Smad3) in rats with heart failure and heart failure after ischemia-reperfusion

and the intervention effect of Dendrobii Officinalis Caulis (DOC) myocardial fibrosis in model rats.

Method:

A rat model of heart failure and Qi deficiency was established through ligation of the left anterior descending coronary artery. The rats were divided into blank group

model group

valsartan group (9.43 mg·kg

-1

) and DOC group (10 mg·kg

-1

)

with 10 in each group. The blank group and the model group were given an equal volume of physiological saline. The changes in left ventricular end-diastolic diameter (LVEDD)

left ventricular end-systolic dimension(LVESD)

left ventricular ejection fraction (LVEF)

left ventricular fractional shortening (LVFS) of the cardiac cycle of rats in each group were recorded by high-resolution ultrasound system. The carboxyterrninal propeptide of type I procollagen (PICP)

and carboxyterrninal propeptide of type Ⅲ procollagen (PIIINP)were detected by enzyme-linked immunosorbent assay (ELISA) kit. The morphological changes of myocardial cells were observed by hematoxylin-eosin (HE) staining. The changes of myocardial fiber tissue and collagen were observed by Masson staining. Western blot was used to detect the protein expressions of Gal-3

TGF-

Smad3.

Result:

Compared with the blank group

the levels of LVEDD

LVEF

and LVFS were lower in the model group (

0.05)

the levels of LVESD

PICP and PIIINP were increased (

0.05)

while the expression levels of Gal-3

TGF-

and Smad3 were decreased (

0.05). Compared with the model group

LVEDD

LVEF

LVFS of the control group and the experimental group were better than the model group (

0.05)

and LVESD

PICP

PIIINP levels of the experimental group were lower than the control group (

0.05)

LVESD

PPIC

PIIINP were lower than those of the model group (

0.05)

expression levels of Gal-3

TGF-

and Smad3 were lower than those in the model group (

0.05)

and the experimental group was lower than the control group (

0.05). According to HE staining

the morphological changes in myocardial cells in the experimental group were more significant than that in the control group. Masson staining showed that the morphological changes of myocardial fibrous tissue and collagen tissue in the experimental group were more significant than that in the control group.

Conclusion:

DOC can effectively inhibit myocardial fibrosis in rats with heart failure and heart Qi deficiency syndrome after ischemia-reperfusion. The mechanism may be correlated with the reduction of the expressions of Gal-3

TGF-

and Smad3.

关键词

Keywords

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