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Open AccessArticle

Lebetin 2, a Snake Venom-Derived B-Type Natriuretic Peptide, Provides Immediate and Prolonged Protection against Myocardial Ischemia-Reperfusion Injury via Modulation of Post-Ischemic Inflammatory Response

1
Laboratoire des Venins et Biomolécules Thérapeutiques (LR11IPT08) et Plateforme de Physiologie et de Physiopathologie Cardiovasculaires (P2C), Institut Pasteur de Tunis, Université Tunis El Manar, 1068 Tunis, Tunisia
2
Université Carthage Tunis, 1054 Bizerte, Tunisia
3
Normandie Univ, UNIROUEN, Inserm U1096, FHU REMOD-VHF, 76000 Rouen, France
4
Université Grenoble Alpes, Inserm U1042, Laboratoire HP2, 38000 Grenoble, France
*
Author to whom correspondence should be addressed.
Toxins 2019, 11(9), 524; https://doi.org/10.3390/toxins11090524
Received: 19 July 2019 / Revised: 8 August 2019 / Accepted: 16 August 2019 / Published: 10 September 2019
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 and fibrosis have not been defined. Here, we determined whether a single L2 injection exerts cardioprotection in IR murine models in vivo, and whether inflammatory response to ischemic injury plays a role in L2-induced effects. We quantified infarct size (IS), fibrosis, inflammation, and both endothelial cell and cardiomyocyte densities in injured myocardium and compared these values with those induced by B-type natriuretic peptide (BNP). Both L2 and BNP reduced IS, fibrosis, and inflammatory response after IR, as evidenced by decreased leukocyte and proinflammatory M1 macrophage infiltrations in the infarcted area compared to untreated animals. However, only L2 increased anti-inflammatory M2-like macrophages. L2 also induced a higher density of endothelial cells and cardiomyocytes. Our data show that L2 has strong, acute, prolonged cardioprotective effects in post-MI that are mediated, at least in part, by the modulation of the post-ischemic inflammatory response and especially, by the enhancement of M2-like macrophages, thus reducing IR-induced necrotic and fibrotic effects. View Full-Text
Keywords: natriuretic peptide; myocardial infarction; ischemia-reperfusion injury; inflammation; fibrosis natriuretic peptide; myocardial infarction; ischemia-reperfusion injury; inflammation; fibrosis
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Tourki, B.; Dumesnil, A.; Belaidi, E.; Ghrir, S.; Godin-Ribuot, D.; Marrakchi, N.; Richard, V.; Mulder, P.; Messadi, E. Lebetin 2, a Snake Venom-Derived B-Type Natriuretic Peptide, Provides Immediate and Prolonged Protection against Myocardial Ischemia-Reperfusion Injury via Modulation of Post-Ischemic Inflammatory Response. Toxins 2019, 11, 524.

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