CN: 32-1845/R
ISSN: 2095-6975
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MENG Zheng-Jie, WANG Chao, MENG Ling-Tong, BAO Bei-Hua, WU Jin-Hui, HU Yi-Qiao. Sodium tanshinone ⅡA sulfonate attenuates cardiac dysfunction and improves survival of rats with cecal ligation and puncture-induced sepsis[J]. Chinese Journal of Natural Medicines, 2018, 16(11): 846-855

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

MENG Zheng-Jie1,2, WANG Chao3, MENG Ling-Tong2, BAO Bei-Hua4, WU Jin-Hui2, HU Yi-Qiao2
1 College of Biotechnology and Pharmaceutical Engineering, Nanjing Tech University, Nanjing 211816, China;
2 State Key Laboratory of Pharmaceutical Biotechnology, Medical School, Nanjing University, Nanjing 210093, China;
3 School of Pharmaceutical Sciences, Nanjing Tech University, Nanjing 211816, China;
4 Jiangsu Key Laboratory for High Technology of Traditional Chinese Medicine Formulae Research, College of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China
Abstract:
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.
Key words:    Sodium tanshinone ⅡA sulfonate    Sepsis    Cardiac dysfunction    Cytokine    Cecal ligation and puncture model   
Received: 2017-05-18   Revised:
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Articles by MENG Zheng-Jie
Articles by WANG Chao
Articles by MENG Ling-Tong
Articles by BAO Bei-Hua
Articles by WU Jin-Hui
Articles by HU Yi-Qiao
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