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Phytomedicine. 2019 Apr;57:255-261. doi: 10.1016/j.phymed.2018.12.040. Epub 2018 Dec 31.

Cardioprotection of salvianolic acid B and ginsenoside Rg1 combination on subacute myocardial infarction and the underlying mechanism.

Author information

1
Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China; School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450001, Henan, China.
2
Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
3
Departments of Vascular Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
4
Agricultural University of Hebei Province, Baoding 071001, Hebei, China.
5
Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China; Agricultural University of Hebei Province, Baoding 071001, Hebei, China.
6
Takarazuka University of Medical and Health Care, Hanayashiki-Midorigaoka, Takarazuka City 6660162, Japan.
7
School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450001, Henan, China. Electronic address: huyr@zzu.edu.cn.
8
Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China. Electronic address: jiangbh@simm.ac.cn.

Abstract

BACKGROUND:

Following myocardial infarction (MI), a series of structural and functional changes evolves in the myocardium, collectively defined as cardiac remodeling.

PURPOSE:

The aim of present study was to investigate the cardioprotection of salvianolicacid B (SalB) and ginsenoside Rg1 (Rg1) combination against cardiac remodeling in a rat model at the subacute phase of MI and further elucidate the underlying mechanism.

METHODS:

Rat heart was exposed via a left thoracotomy at the fourth intercostal space and MI was induced by a ligature below the left descending coronary artery. Hemodynamic assay was conducted using a Mikro-tipped SPR-320 catheter which was inserted through the right carotid artery into left ventricle.Myocardial infarct size was detected using 3,5-triphenyltetrazolium chloride (TTC) staining. Haematoxylin and eosin (HE) stain and picric sirius red stain were conducted for histopathological detection. Immunohistochemistry was used to detect the expression of α-smooth muscle actin (α-SMA) and gelatin zymography was used to evaluate the activities of matrix metalloproteinase-9 (MMP-9).

RESULTS:

Comparing with MI rats, 30 mg/kg SalB-Rg1 improved cardiac function verified by maximum rate of pressure development for contraction (+dp/dtmax, p < 0.01) and maximum rate of pressure development for relaxation (-dp/dtmax, p < 0.05); reduced myocardial infarct size (p < 0.05) verified by TTC staining, improved cardiac structure based on HE stain; decreased collagen volume fraction (p < 0.05) and collagen I/III ratio (p < 0.05) according picrosirius red staining. The underlying mechanism of SalB-Rg1 against cardiac remodeling was associated with its down-regulation on α-SMA expression according immunohistochemistry (p < 0.01) and inhibition on MMP-9 activity based on in-gel zymography (p < 0.05).

CONCLUSION:

All above study indicated the potential therapeutic effects of SalB-Rg1 on heart.

KEYWORDS:

Cardiac remodeling; Ginsenoside Rg1; Myocardial fibrosis; Myocardialinfarction; Salvianolic acid B

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