Protective Effect of a Novel Polysaccharide from Lonicera japonica on Cardiomyocytes of Mice Injured by Hydrogen Peroxide.

Xiaonan Zhou,Gui He,Xun Gong,Min Tang,Jinming Ma,Ling Kui,Huajun Zhang,Geng Tian

doi:10.1155/2020/5279193

Abstract

Lonicera japonica is a traditional Chinese herbal medicine with antioxidation, anti-inflammatory, antibacterial, and immunoregulation functions. A method to isolate polysaccharides from Lonicera japonica (LJP) has been reported previously by our group. We also reported previously that LJP was consisted of 6 types of monosaccharides and had the characteristic absorption of typical polysaccharides. In this study, we investigated the protective effect of LJP on cardiomyocytes of mice injured by hydrogen peroxide (H2O2). The results showed that LJP can increase the cardiomyocyte viability and the activities of the enzyme (SOD, CAT, GSH-Px, AST, CPK, and LDH) in cardiomyocytes of mice injured by hydrogen peroxide. The results of intracellular ROS contents showed that a high dose (40 μg mL−1) of LJP had the best effects on protecting the cardiomyocytes of mice injured by H2O2. In addition, the measurement results of the cardiomyocyte apoptosis and the activity of caspase-3, caspase-8, and caspase-9 in cardiomyocytes confirmed this conclusion from another perspective.

Highlights

Coronary heart disease and acute myocardial infarction increased year by year, which has become one of the major diseases endangering human life and health [1, 2]
The cardiomyocyte survival rate of the Lonicera japonica (LJP) group raised significantly compared with the H2O2 group (P < 0:05)
The results suggest that oral administration of the LJP is able to add the cardiomyocyte survival rate of oxidative stress

Summary

Introduction

Coronary heart disease and acute myocardial infarction increased year by year, which has become one of the major diseases endangering human life and health [1, 2]. In a variety of cardiovascular diseases, such as myocardial infarction and ischemia-reperfusion injury, cardiomyocytes were found to be injured. The pathological mechanism of cardiomyocyte injury is complex, of which peroxidation damage is one of the main factors that cause myocardial injury [3,4,5]. Peroxidation of myocardial cells can damage the structure of the biofilm, increase mitochondrial permeability, and thereby affect cell function. When oxidative stress more than a certain intensity of injury, myocardial cells will be irreversible damaged such as apoptosis and necrosis [6,7,8]. Looking for antioxidation drugs to reduce oxidative stress-induced myocardial injury is of great significance

Methods

Results

Conclusion