Abstract
Purpose: To investigate the protective effect of trigonoside II against sepsis-induced myocardial injury in rats, and the mechanism involved.
 Methods: Adult male Sprague Dawley rats (n = 30) weighing 200 - 230 g (mean weight = 215 ± 15 g) were used for this study. The rats were randomly assigned to 3 groups (10 rats/group): sham, cecal ligation puncture (CLP), and trigonoside II. Rats in the treatment group received trigonoside II at a dose of 2 mg/kg intraperitoneally (i.p.) at 3, 12 and 24 h post-surgery. Sepsis was induced using CLP method. Lactate dehydrogenase (LDH) and creatine kinase (CK-MB) activities, and hemodynamic functions were determined in the rats. The levels of interleukin (IL)-1β and IL-6, and tumor necrosis factor α (TNF-α) were assayed in rat serum. Oxidative stress and myocardial cell apoptosis were determined by measuring malondialdehyde (MDA) levels, while activities of glutathione peroxidase (GPx), superoxide dismutase (SOD) and myeloperoxidase (MPO), as well as levels of expression of bax, bcl-2 and caspase-3 were also assessed.
 Results: Treatment of myocardial injury rats with trigonoside II led to significant reductions in the activities of LDH, CK-MB and MPO, and decreases in levels of IL-1β, IL-6 and TNF-α (p < 0.05). It also significantly reversed the effects of sepsis on rat hemodynamic functions (p < 0.05). Trigonoside IItreatment significantly reduced MDA levels in rat myocardial tissues, but significantly increased SOD and GPx activities (p < 0.05). It significantly down-regulated protein expressions of NF-kB and TLR-4 in myocardial tissues (p < 0.05). The number of apoptotic cells and activity of caspase-3 were significant increased in myocardial tissues of rats in CLP group, when compared with sham group, but were reduced significantly in myocardial tissues of trigonoside II-treated rats (p < 0.05). Similarly, trigonoside II treatment down-regulated the protein expressions of caspase-3 and bax, but upregulated bcl-2 protein expression in the rat myocardial tissues (p < 0.05).
 Conclusion: The results of this study indicate that trigonoside II confers protection on sepsis-induced myocardial injury via reduction in oxidative stress and regulation of TLR-4/NF-kB inflammatory pathway.
 Keywords: Cecal ligation puncture, Myocardial injury, Oxidative stress, Sepsis, Trigonoside II
Highlights
Sepsis occurs when chemicals released in the bloodstream to fight an infection trigger inflammation
Treatment of myocardial injury rats with trigonoside II led to significant reductions in the activities of Lactate dehydrogenase (LDH) and CK-MB (p < 0.05; Figure 1)
Myocardial tissues were trypsinized with 10 % trypsin and the resultant cell suspension was washed twice with phosphate-buffered saline (PBS) and lysed with 250 μL of ice-cold radioimmunoprecipitation assay (RIPA) buffer containing protease and phosphatase inhibitors
Summary
Sepsis occurs when chemicals released in the bloodstream to fight an infection trigger inflammation. This causes a cascade of changes that damage multiple organ systems, making them to fail, sometimes even resulting in death [1]. Heme oxygenase-1 (HO-1), a heat-stable protein that regulates oxidative stress, has been shown to reduce myocardial injury [5]. It activates Nrf-2, a basic leucine zipper (bZIP) protein that regulates the expression of antioxidant proteins which protect tissues against oxidative damage triggered by injury and inflammation. The aim of this study was to investigate the protective effect of trigonoside II against sepsis-induced myocardial injury in rats, and the mechanism involved
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