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Abstract
ABSTRACTPurposeThe present study explored the potential therapeutic role of oleuropein in sepsis-induced heart injury along with the role of GSK-3β/NF-kB signaling pathway.MethodsSepsis-induced myocardial injury was induced by cecal ligation and puncture (CLP) in rats. The cardiac injury was assessed by measuring the levels of cTnI and creatine kinase-MB (CK-MB). Sepsis-induced inflammation was assessed by measuring interleukin-6 (IL-6), IL-10 and HMGB1 levels. The different doses of oleuropein (5, 10, and 20 mg/kg) were given prior to CLP. Oleuropein (20 mg/kg) was administered after 6 hof CLP. The expressions of GSK-3β, p-GSK-3β (Ser9) and nuclear factor-κB (NF-κB) were measured in heart homogenates.ResultsCecal ligation and puncture was associated with myocardial injury, an increase in IL-6, a decrease in IL-10 and an increase in HMGB1. Moreover, it decreased the ratio of p-GSK-3β/GSK-3β and increased the expression of p-NF-kB. Pretreatment with oleuropein attenuated CLP-induced myocardial injury and systemic inflammation in a dose-dependent manner. Administration of oleuropein after the onset of CLP also attenuated cardiac injury and inflammation. It also restored CLP-induced changes in the HMGB1 levels, the ratio of p-GSK-3β/GSK-3β and expression of p- NF-kB.ConclusionsOleuropein attenuates sepsis-induced systemic inflammation and myocardial injury by inhibiting NF-kB and GSK-3β signaling.
Highlights
Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection[1]
Cecal ligation puncture produced myocardial injury and increased systemic inflammation The ligation and puncture of the cecum led to marked myocardial injury, which was assessed 12 h after laparotomy
cecal ligation and puncture (CLP) induced systemic inflammation and there was a significant increase in the plasma levels of proinflammatory cytokine, IL-6 (Fig. 3) and decrease in the plasma levels of anti-inflammatory cytokine, IL-10 (Fig. 4)
Summary
Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection[1]. Sepsis may induce widespread damage in the different body organs including the myocardium[3]. Myocardial dysfunction is very common in patients suffering from sepsis and it is recognized as one of the major health burdens throughout the world, which may contribute to morbidity as well as mortality. The release of heart-specific biomarkers, including cardiac troponins and creatine kinase, is employed to assess sepsis-induced myocardial injury[4,5]. There is specific drug therapy for the management of sepsis-induced myocardial injury. There is a need to explore new therapeutic agents that may be potentially employment for the successful mitigation of the myocardial injury in sepsis patients
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