Protective effects of the melanocortin analog NDP-α-MSH in rats undergoing cardiac arrest
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We previously reported that melanocortins afford cardioprotection in conditions of experimental myocardial ischemia/reperfusion, with involvement of the janus kinases (JAK), extracellular signal-regulated kinases (ERK) and signal transducers and activators of transcription (STAT) signalings. We investigated the influence of the melanocortin analog [Nle(4), D-Phe(7)]α-melanocyte-stimulating hormone (NDP-α-MSH) on short-term detrimental responses to cardiac arrest (CA) induced in rats by intravenous (i.v.) administration of potassium chloride, followed by cardiopulmonary resuscitation (CPR) plus epinephrine treatment. In CA/CPR rats i.v. treated with epinephrine (0.1 mg/kg) and returned to spontaneous circulation (48%) we recorded low values of mean arterial pressure (MAP) and heart rate (HR), alteration of hemogasanalysis parameters, left ventricle low expression of the cardioprotective transcription factors pJAK2 and pTyr-STAT3 (JAK-dependent), increased oxidative stress, up-regulation of the inflammatory mediators tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), and down-regulation of the anti-inflammatory cytokine IL-10, as assessed at 1h and 3h after CPR. On the other hand, i.v. treatment during CPR with epinephrine plus NDP-α-MSH (340 μg/kg) almost completely restored the basal conditions of MAP and HR, reversed metabolic acidosis, induced left ventricle up-regulation of pJAK2, pTyr-STAT3 and IL-10, attenuated oxidative stress, down-regulated TNF-α and IL-6 levels, and improved survival rate by 81%. CA/CPR plus epinephrine alone or in combination with NDP-α-MSH did not affect left ventricle pSer-STAT3 (ERK1/2-dependent) and pERK1/2 levels. These results indicate that melanocortins improve return to spontaneous circulation, reverse metabolic acidosis, and inhibit heart oxidative stress and inflammatory cascade triggered by CA/CPR, likely via activation of the JAK/STAT signaling pathway.
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- Authors
- Ottani, A., Neri, L., Canalini, F., Calevro, A., Rossi, R., Cappelli, G., Ballestri, M., Giuliani, D., & Guarini, S.
- Affiliations
- University of Modena and Reggio Emilia (IT)
- Corresponding author
- Giuliani, Daniela
- Guarini, Salvatore
- ORCID
- Venue
- European Journal of Pharmacology
- Publisher
- Elsevier BV
- Published
- 2014-12
- Volume
- 745
- Pages
- 108-116
- ISSN
- 0014-2999 (ISSN-L)
- OpenAlex
- W2072059041
- Cited by
- 19
- References
- 52
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 2 · 2018: 1 · 2017: 7 · 2016: 1 · 2015: 2
- FWCI
- 3.57
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Locations
- European Journal of Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- IRIS UNIMORE (University of Modena and Reggio Emilia) (submittedVersion, cc-by)
- Funders
- Department of Biomedical, Metabolic and Neural Sciences of University of Modena and Reggio Emilia, Italy
- Topics
- Health Sciences › Medicine › Emergency Medicine › Cardiac Arrest and Resuscitation
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- cardiac arrest, cardioprotection, cardiopulmonary resuscitation, epinephrine, JAK/STAT signaling, STAT3, JAK2, oxidative stress, inflammation, TNF-α, interleukin-6, IL-10, metabolic acidosis, myocardial ischemia-reperfusion injury
- MeSH terms
- alpha-MSH, Animals, Carbon Dioxide, Cardiotonic Agents, Epinephrine, Heart Arrest, Hemodynamics, Male, Oxygen, Signal Transduction, Cytokines, Cardiopulmonary Resuscitation, Rats, Sprague-Dawley, Apoptosis, Oxidative Stress, Inflammation Mediators, MAP Kinase Signaling System, STAT3 Transcription Factor, Rats, Melanocortins, Janus Kinase 2
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