Research Papers:

Cardioprotective properties of N-terminal galanin fragment (2-15) in experimental ischemia/reperfusion injury

Oleg Pisarenko, Andrei Timotin, Maria Sidorova, Irina Studneva, Valentin Shulzhenko, Marina Palkeeva, Larisa Serebryakova, Aleksander Molokoedov, Oksana Veselova, Mathieu Cinato, Frederic Boal, Helene Tronchere and Oksana Kunduzova _

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Oncotarget. 2017; 8:101659-101671. https://doi.org/10.18632/oncotarget.21503

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Oleg Pisarenko1,*, Andrei Timotin2,3,*, Maria Sidorova1, Irina Studneva1, Valentin Shulzhenko1, Marina Palkeeva1, Larisa Serebryakova1, Aleksander Molokoedov1, Oksana Veselova1, Mathieu Cinato2,3, Frederic Boal2,3, Helene Tronchere2,3 and Oksana Kunduzova2,3,*

1Russian Cardiology Research and Production Complex, Moscow, Russian Federation

2National Institute of Health and Medical Research (INSERM) U1048, Toulouse, France

3University of Toulouse, UPS, Institute of Metabolic and Cardiovascular Diseases, Toulouse, France

*These authors have contributed equally to this work

Correspondence to:

Oksana Kunduzova, email: [email protected]

Keywords: galanin (2-15); apoptosis; cardiac injury; energy metabolism; oxidative stress

Received: August 02, 2017    Accepted: September 04, 2017    Published: October 05, 2017


Background and purpose: Galanin is an endogenous peptide involved in diverse physiological functions in the central nervous system including central cardiovascular regulation. The present study was designed to evaluate the potential effects of the short N-terminal galanin fragment 2-15 (G) on cardiac ischemia/reperfusion (I/R) injury.

Experimental Approach: Peptide G was synthesized by the automatic solid phase method and identified by 1H-NMR spectroscopy and mass spectrometry. Experiments were performed on cultured rat cardiomyoblast (H9C2) cells, isolated perfused working rat hearts and anaesthetized open-chest rats.

Key Results: Cell viability increased significantly after treatment with 10 and 50 nM of G peptide. In hypoxia and reoxygenation conditions, exposure of H9C2 cells to G peptide decreased cell apoptosis and mitochondrial reactive oxygen species (ROS) production. Postischemic infusion of G peptide reduced cell membrane damage and improved functional recovery in isolated hearts during reperfusion. These effects were accompanied by enhanced restoration of myocardial metabolic state. Treatment with G peptide at the onset of reperfusion induced minor changes in hemodynamic variables but significantly reduced infarct size and plasma levels of necrosis markers.

Conclusion and implications: These findings suggest that G peptide is effective in mitigating cardiac I/R injury, thereby providing a rationale for promising tool for the treatment of cardiovascular diseases.

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