Yanqing Guo1, Jiyao Xu1, Yongzhi Deng2, Li Wu1, Jingping Wang1, Jian An1. 1. Department of Cardiology, Shanxi Cardiovascular Hospital, Taiyuan, China. 2. Department of Cardiovascular Surgery, Shanxi Cardiovascular Hospital, Taiyuan, China.
Abstract
BACKGROUND: Abnormal Ca2+ circulation in cardiomyocytes is an important cause of decreased myocardial contractility in failing hearts. Nitroxyl hydrogen (HNO) can oxidize Ca2+ cycle-related proteins, alter their biological functions, promote Ca2+ recovery as well as release, and enhance myocardial contractility. In this study, we aim to observe the effect of nitrosyl hydrogen (HNO) on the cardiac function of rats with heart failure and elucidate the underlying mechanism. METHODS: Twenty six male Wistar rats were randomly divided into heart failure group (HF group), Angeli's salt treatment group (HF + AS group) and sham operation group (Sham group). The HF + AS group rats were treated with HNO donor Angeli's salt by intraperitoneal injection of 1 mg/kg/d, and the rats in the HF group and the Sham group were given the same amount of normal saline. Cardiac function was measured by echocardiography before and after treatment. NT-proBNP was measured by enzyme immunoassay (ELISA) kit after treatment. Western blot were used to measure the expression of sarcoplasmic reticulum Ca2+-ATPase (SERCA) in protein levels in rats. The activities of SERCA2a were detected by the biochemical kit finally. RESULTS: We found that Nitrosyl hydrogen could significantly increase LVEF, +dp/dt, -dp/dt (P<0.05), significantly decrease NT-ProBNP and LVEDP (P<0.01), and significantly enhance the activities of SERCA2a protein (P<0.05). CONCLUSIONS: These findings suggest that Nitrosyl hydrogen could improve the cardiac function possibly by increasing protein activities of SERCA2a in rats. 2020 Cardiovascular Diagnosis and Therapy. All rights reserved.
BACKGROUND: Abnormal Ca2+ circulation in cardiomyocytes is an important cause of decreased myocardial contractility in failing hearts. Nitroxyl hydrogen (HNO) can oxidize Ca2+ cycle-related proteins, alter their biological functions, promote Ca2+ recovery as well as release, and enhance myocardial contractility. In this study, we aim to observe the effect of nitrosyl hydrogen (HNO) on the cardiac function of rats with heart failure and elucidate the underlying mechanism. METHODS: Twenty six male Wistar rats were randomly divided into heart failure group (HF group), Angeli's salt treatment group (HF + AS group) and sham operation group (Sham group). The HF + AS group rats were treated with HNO donor Angeli's salt by intraperitoneal injection of 1 mg/kg/d, and the rats in the HF group and the Sham group were given the same amount of normal saline. Cardiac function was measured by echocardiography before and after treatment. NT-proBNP was measured by enzyme immunoassay (ELISA) kit after treatment. Western blot were used to measure the expression of sarcoplasmic reticulum Ca2+-ATPase (SERCA) in protein levels in rats. The activities of SERCA2a were detected by the biochemical kit finally. RESULTS: We found that Nitrosyl hydrogen could significantly increase LVEF, +dp/dt, -dp/dt (P<0.05), significantly decrease NT-ProBNP and LVEDP (P<0.01), and significantly enhance the activities of SERCA2a protein (P<0.05). CONCLUSIONS: These findings suggest that Nitrosyl hydrogen could improve the cardiac function possibly by increasing protein activities of SERCA2a in rats. 2020 Cardiovascular Diagnosis and Therapy. All rights reserved.
Authors: Karen L Andrews; Amanda K Sampson; Jennifer C Irvine; Waled A Shihata; Danielle L Michell; Natalie G Lumsden; Chloe Lim; Olivier Huet; Grant R Drummond; Barbara K Kemp-Harper; Jaye P F Chin-Dusting Journal: Clin Sci (Lond) Date: 2016-05-26 Impact factor: 6.124
Authors: Carlo G Tocchetti; Brian A Stanley; Christopher I Murray; Vidhya Sivakumaran; Sonia Donzelli; Daniele Mancardi; Pasquale Pagliaro; Wei Dong Gao; Jennifer van Eyk; David A Kass; David A Wink; Nazareno Paolocci Journal: Antioxid Redox Signal Date: 2011-03-03 Impact factor: 8.401