Chuang Li1, Weiguo Wan1, Tianxin Ye1, Yazhou Sun1, Xiaoli Chen1, Xin Liu1, Shaobo Shi1, Yan Zhang1, Chuan Qu1, Bo Yang2, Cui Zhang3. 1. Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, PR China; Cardiovascular Research Institute, Wuhan University, Wuhan 430060, PR China; Hubei Key Laboratory of Cardiology, Wuhan 430060, PR China. 2. Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, PR China; Cardiovascular Research Institute, Wuhan University, Wuhan 430060, PR China; Hubei Key Laboratory of Cardiology, Wuhan 430060, PR China. Electronic address: yybb112@whu.edu.cn. 3. Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, PR China; Cardiovascular Research Institute, Wuhan University, Wuhan 430060, PR China; Hubei Key Laboratory of Cardiology, Wuhan 430060, PR China. Electronic address: cuizhang2005@126.com.
Abstract
AIM: Recent studies have shown that, with its excellent anti-inflammatory and antioxidant effects, pinocembrin can reduce the occurrence of arrhythmia in myocardial infarction rats. However, whether it can alleviate lipopolysaccharide (LPS)-induced myocardial injury in rats has not been reported. Therefore, the purpose of this study was to investigate whether pinocembrin could alleviate myocardial injury and arrhythmia in rats with sepsis. MATERIALS AND METHODS: Rats were intraperitoneally injected with LPS to simulate animal sepsis, and the caudal vein was injected with pinocembrin or normal saline for intervention. Transthoracic echocardiography, inflammatory factors, electrophysiological recording, histological analysis, and western-blot analysis were performed. KEY FINDINGS: Compared with the control group, the rats in the LPS group had myocardial injury and cardiac dysfunction, and the incidence of ventricular arrhythmia increased. In addition, LPS resulted in the increase of p-c-Jun N-terminal kinase (JNK), p-p38 proteins in the myocardium, the levels of inflammatory factors in the blood and the apoptosis rate of left ventricular cardiomyocytes. And all these adverse effects were eliminated, thus confirming that pinocembrin has an excellent protective effect on the heart. SIGNIFICANCE: Reducing the inflammatory response and cell apoptosis by inhibiting p38/JNK mitogen-activated protein kinase (MAPK) signaling pathway, pinocembrin can alleviate myocardial injury, cardiac dysfunction, and ventricular arrhythmia induced by LPS.
AIM: Recent studies have shown that, with its excellent anti-inflammatory and antioxidant effects, pinocembrin can reduce the occurrence of arrhythmia in myocardial infarctionrats. However, whether it can alleviate lipopolysaccharide (LPS)-induced myocardial injury in rats has not been reported. Therefore, the purpose of this study was to investigate whether pinocembrin could alleviate myocardial injury and arrhythmia in rats with sepsis. MATERIALS AND METHODS:Rats were intraperitoneally injected with LPS to simulate animal sepsis, and the caudal vein was injected with pinocembrin or normal saline for intervention. Transthoracic echocardiography, inflammatory factors, electrophysiological recording, histological analysis, and western-blot analysis were performed. KEY FINDINGS: Compared with the control group, the rats in the LPS group had myocardial injury and cardiac dysfunction, and the incidence of ventricular arrhythmia increased. In addition, LPS resulted in the increase of p-c-Jun N-terminal kinase (JNK), p-p38 proteins in the myocardium, the levels of inflammatory factors in the blood and the apoptosis rate of left ventricular cardiomyocytes. And all these adverse effects were eliminated, thus confirming that pinocembrin has an excellent protective effect on the heart. SIGNIFICANCE: Reducing the inflammatory response and cell apoptosis by inhibiting p38/JNK mitogen-activated protein kinase (MAPK) signaling pathway, pinocembrin can alleviate myocardial injury, cardiac dysfunction, and ventricular arrhythmia induced by LPS.