Sodium tanshinone IIA sulfonate attenuates cardiac dysfunction and improves survival of rats with cecal ligation and puncture-induced sepsis

作     者：MENG Zheng-Jie WANG Chao MENG Ling-Tong BAO Bei-Hua WU Jin-Hui HU Yi-Qiao MENG Zheng-Jie;WANG Chao;MENG Ling-Tong;BAO Bei-Hua;WU Jin-Hui;HU Yi-Qiao

作者机构：College of Biotechnology and Pharmaceutical Engineering Nanjing Tech University State Key Laboratory of Pharmaceutical Biotechnology Medical School Nanjing University School of Pharmaceutical Sciences Nanjing Tech University Jiangsu Key Laboratory for High Technology of Traditional Chinese Medicine Formulae Research College of Pharmacy Nanjing University of Chinese Medicine 

出 版 物：《Chinese Journal of Natural Medicines》 (中国天然药物（英文版）)

年 卷 期：2018年第16卷第11期

页      面：846-855页

核心收录：

学科分类：0710[理学-生物学] 1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 1005[医学-中医学] 100706[医学-药理学] 1002[医学-临床医学] 0703[理学-化学] 100602[医学-中西医结合临床] 10[医学] 

主　　题：Sodium tanshinone II A sulfonate Sepsis Cardiac dysfunction Cytokine Cecal ligation and puncture model 

摘      要：Cardiac dysfunction, a common consequence of sepsis, is the major contribution to morbidity and mortality in patients. Sodium tanshinone IIA sulfonate(STS) is a water-soluble derivative of Tanshinone IIA(TA), a main active component of Salvia miltiorrhiza Bunge, which has been widely used in China for the treatment of cardiovascular and cerebral system diseases. In the present study, the effect of STS on sepsis-induced cardiac dysfunction was investigated and its effect on survival rate of rats with sepsis was also evaluated. STS treatment could significantly decrease the serum levels of C-reactive protein(CRP), procalcitonin(PCT), cardiac troponin Ⅰ(cTn-Ⅰ), cardiac troponin T(cTn-T), and brain natriuretic peptide(BNP) in cecal ligation and puncture(CLP)-induced) septic rats and improve left ventricular function, particularly at 48 and 72 h after CLP. As the pathogenesis of septic myocardial dysfunction is attributable to dysregulated systemic inflammatory responses, several key cytokines, including tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), interleukin-6(IL-6), interleukin-10(IL-10) and high mobility group protein B1(HMGB1), were detected to reveal the possible mechanism of attenuation of septic myocardial dysfunction after being treated by STS. Our study showed that STS, especially at a high dose(15 mg×kg–1), could efficiently suppress inflammatory responses in myocardium and reduce myocardial necrosis through markedly reducing production of myocardial TNF-α, IL-6 and HMGB1. STS significantly improved the 18-day survival rate of rats with sepsis from 0% to 30%(P 0.05). Therefore, STS could suppress inflammatory responses and improve left ventricular function in rats with sepsis, suggesting that it may be developed for the treatment of sepsis.