Lin Yang1, Hui Zhang2, Peili Chen3. 1. Department of Critical Care Medicine, The First People's Hospital of Shangqiu, Shangqiu, 476100, China. Electronic address: yangl_sqhospital@sina.com. 2. Department of Critical Care Medicine, The First People's Hospital of Shangqiu, Shangqiu, 476100, China. 3. Department of Critical Care Medicine, The First People's Hospital of Shangqiu, Shangqiu, 476100, China. Electronic address: 1484362246@qq.com.
Abstract
OBJECTIVE: Sulfur dioxide (SO2) plays an important role in maintaining homeostasis of cardiovascular system. This study was aimed to investigate cardioprotective effects of SO2 on in the rat and the underlying mechanism. METHODS AND RESULTS: Sepsis model induced by cecal ligation and puncture (CLP) in rats were used. SO2 donor (NaHSO3/Na2SO3, 1:3 M/M) was administered intraperitoneally at a dose of 85 mg/kg. Primary neonatal rat cardiac ventricular myocytes (NRCMs) were stimulated with LPS (1 mg/mL) in presence or absence of different concentrations of SO2 (10, 50 and 100 μmol/L). SO2 donor could restore the decreased levels of SO2 in plasma and heart of septic rats. SO2 exhibited dramatic improvement in cardiac functions. At 24 h after CLP, SO2 treatments decreased the number of TUNEL-positive cells, Bax/Bcl-2 ratio and activity of caspase-3. Moreover CLP-induced inflammatory response was also relieved by SO2. In NRCMs, SO2 could suppress the LPS-induced myocardial injury, leading to an increase in cell viability, a decrease in LDH and apoptotic rate. Western blot showed that the expression of TLR4, NLRP3, and Caspase-1 were obviously increased in myocardial tissue of CLP group or in NRCMs of LPS group, while SO2 significantly inhibited the CLP-induced or LPS-induced TLR4, NLRP3, and Caspase-1 expression. CONCLUSION: SO2 attenuated sepsis-induced cardiac dysfunction likely in association with the inhibiting inflammation via TLR4/NLRP3 signaling pathway.
OBJECTIVE:Sulfur dioxide (SO2) plays an important role in maintaining homeostasis of cardiovascular system. This study was aimed to investigate cardioprotective effects of SO2 on in the rat and the underlying mechanism. METHODS AND RESULTS: Sepsis model induced by cecal ligation and puncture (CLP) in rats were used. SO2donor (NaHSO3/Na2SO3, 1:3 M/M) was administered intraperitoneally at a dose of 85 mg/kg. Primary neonatal rat cardiac ventricular myocytes (NRCMs) were stimulated with LPS (1 mg/mL) in presence or absence of different concentrations of SO2 (10, 50 and 100 μmol/L). SO2donor could restore the decreased levels of SO2 in plasma and heart of septic rats. SO2 exhibited dramatic improvement in cardiac functions. At 24 h after CLP, SO2 treatments decreased the number of TUNEL-positive cells, Bax/Bcl-2 ratio and activity of caspase-3. Moreover CLP-induced inflammatory response was also relieved by SO2. In NRCMs, SO2 could suppress the LPS-induced myocardial injury, leading to an increase in cell viability, a decrease in LDH and apoptotic rate. Western blot showed that the expression of TLR4, NLRP3, and Caspase-1 were obviously increased in myocardial tissue of CLP group or in NRCMs of LPS group, while SO2 significantly inhibited the CLP-induced or LPS-induced TLR4, NLRP3, and Caspase-1 expression. CONCLUSION:SO2 attenuated sepsis-induced cardiac dysfunction likely in association with the inhibiting inflammation via TLR4/NLRP3 signaling pathway.
Authors: Michael L'Heureux; Michael Sternberg; Lisa Brath; Jeremy Turlington; Markos G Kashiouris Journal: Curr Cardiol Rep Date: 2020-05-06 Impact factor: 2.931