Bochra Tourki

• PhD Student at Institut Pasteur de Tunis

Introduction: Age-related cardiac dysfunction is a prime component of sepsis-induced multi-organ failure in the clinical setting. Arachidonate 5-lipoxygenase (5LOX) pathway and 5LOX-derived lipid mediators are critical in early inflammation and immune response signaling. In addition, 5LOX derived mediators activate macrophages and other cells to co...

Heart failure with preserved ejection fraction (HFpEF) is an emerging disease with signs of nonresolving inflammation, endothelial dysfunction, and multiorgan defects. Moreover, based on the clinical signs and symptoms and the rise of the obesity epidemic, the number of patients developing HFpEF is increasing. From recent molecular and cellular stu...

The presistent increase of 12/15 lipoxygenase enzyme activity is correlated with uncontrolled inflammation, leading to organ dysfunction. ML351, a potent 12/15 lipoxygenase (12/15LOX) inhibitor, was reported to reduce infarct size and inflammation in a murine ischemic stroke model. In the presented work, we have applied three complementary experime...

Chronic unresolved inflammation is the primary determinant of cardiovascular disease. Precise mechanisms that define the genesis of unresolved inflammation in heart failure with preserved ejection fraction (HFpEF) are of interest due to the obesity epidemic. To examine the obesity phenotype and its direct/indirect consequences, multiple approaches...

Objective: Recently, we observed that the specialized proresolving mediator (SPM) entity resolvin D1 activates lipoxin A4/formyl peptide receptor 2 (ALX/FPR2), which facilitates cardiac healing and persistent inflammation is a hallmark of impaired cardiac repair in aging. Splenic leukocyte-directed SPMs are essential for the safe clearance of infl...

After myocardial infarction, splenic leukocytes direct biosynthesis of specialized pro-resolving mediators (SPMs) that are essential for the resolution of inflammation and tissue repair. In a laboratory environment, after coronary ligation of healthy risk free rodents (young adult mice) leukocytes biosynthesize SPMs with induced activity of lipoxyg...

Myocardial infarction (MI) followed by left ventricular (LV) remodeling is the most frequent cause of heart failure. Lebetin 2 (L2), a snake venom-derived natriuretic peptide, exerts cardioprotection during acute myocardial ischemia-reperfusion (IR) ex vivo. However, its effects on delayed consequences of IR injury, including post-MI inflammation a...

Cardiac ischemia is one of the leading causes of death worldwide. It is now well established that natriuretic peptides can attenuate the development of irreversible ischemic injury during myocardial infarction. Lebetin 2 (L2) is a new discovered peptide isolated from Macrovipera lebetina venom with structural similarity to B-type natriuretic peptid...

Aims Myocardial infarction (MI) is associated with inflammatory promoting cell death and subsequent fibrosis leading to cardiac dysfunction. Here, we aimed at testing if Lebetin 2 (L2), a snake venom-derived natriuretic peptide and B-type natriuretic peptide (BNP), modulate inflammatory response to ischemia-reperfusion (IR) injury in rats. Methods...

Introduction In this study, we aimed at testing the therapeutic potential of a novel Natriuretic Peptide (NPs), identified from Tunisian snake venom, when administered during reperfusion. Materials and Methods Langendorff perfused male Wistar rat hearts were subjected to 30min regional coronary artery occlusion followed by 90min reperfusion. Heart...