Cilostazol Mediates Immune Responses and Affects Angiogenesis During the Acute Phase of Hind Limb Ischemia in a Mouse Model.


Journal

Journal of cardiovascular pharmacology and therapeutics
ISSN: 1940-4034
Titre abrégé: J Cardiovasc Pharmacol Ther
Pays: United States
ID NLM: 9602617

Informations de publication

Date de publication:
05 2020
Historique:
pubmed: 8 1 2020
medline: 7 10 2020
entrez: 8 1 2020
Statut: ppublish

Résumé

Cilostazol is a drug of choice for the treatment of intermittent claudication that also affects innate and adaptive immune cells. The purpose of our study was the evaluation of cilostazol's impact on the immune and angiogenic response in murine models of hind limb ischemia. We used 108 immunodeficient NOD.CB17-Prkdcscid/J mice and 108 wild-type CB17 mice. At day 0 (D0), all animals underwent hind limb ischemia. Half of them in both groups received daily cilostazol starting at D0 and for the next 7 postoperative days, while the rest of them served as controls, receiving vehicle. Interleukin (IL) 2, IL-4, IL-6, IL-10, IL-17A, tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ) serum concentrations were measured by flow cytometry on postsurgery days D1, D3, D5, and D7. On D7, both groups underwent positron emission tomography scan with There was a statistically significant augmentation ( Cilostazol seems to significantly increase angiogenesis in wild-type animals during the first postoperational week. It also influences immune cells, altering the type of immune response by promoting anti-inflammatory cytokine production in wild-type animals, while it helps toward inflammation regression in immunodeficient animals.

Sections du résumé

BACKGROUND
Cilostazol is a drug of choice for the treatment of intermittent claudication that also affects innate and adaptive immune cells. The purpose of our study was the evaluation of cilostazol's impact on the immune and angiogenic response in murine models of hind limb ischemia.
METHODS
We used 108 immunodeficient NOD.CB17-Prkdcscid/J mice and 108 wild-type CB17 mice. At day 0 (D0), all animals underwent hind limb ischemia. Half of them in both groups received daily cilostazol starting at D0 and for the next 7 postoperative days, while the rest of them served as controls, receiving vehicle. Interleukin (IL) 2, IL-4, IL-6, IL-10, IL-17A, tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ) serum concentrations were measured by flow cytometry on postsurgery days D1, D3, D5, and D7. On D7, both groups underwent positron emission tomography scan with
RESULTS
There was a statistically significant augmentation (
CONCLUSION
Cilostazol seems to significantly increase angiogenesis in wild-type animals during the first postoperational week. It also influences immune cells, altering the type of immune response by promoting anti-inflammatory cytokine production in wild-type animals, while it helps toward inflammation regression in immunodeficient animals.

Identifiants

pubmed: 31906705
doi: 10.1177/1074248419897852
doi:

Substances chimiques

Angiogenesis Inducing Agents 0
Cytokines 0
Inflammation Mediators 0
Cilostazol N7Z035406B

Types de publication

Comparative Study Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

273-285

Auteurs

Efthymios Paronis (E)

Center of Clinical, Experimental Surgery & Translational Research, Biomedical Research Foundation, Academy of Athens (BRFAA), Athens, Greece.
Vascular Surgery Department, School of Medicine, National and Kapodistrian University of Athens, Attikon Teaching Hospital, Athens, Greece.
Section of Animal and Human Physiology, Department of Biology, National and Kapodistrian University of Athens, Panepistimiopolis, Ilissia, Athens, Greece.

Michalis Katsimpoulas (M)

Center of Clinical, Experimental Surgery & Translational Research, Biomedical Research Foundation, Academy of Athens (BRFAA), Athens, Greece.

Nikolaos P E Kadoglou (NPE)

Center for Statistics in Medicine-Botnar Research Centre, University of Oxford, Oxford, United Kingdom.

Claire Provost (C)

Sorbonne University, UMS28, plateforme LIMP, Laboratoire d'Imagerie Moléculaire Positonique, Hopital Tenon, Paris, France.

Marianna Stasinopoulou (M)

Center of Clinical, Experimental Surgery & Translational Research, Biomedical Research Foundation, Academy of Athens (BRFAA), Athens, Greece.

Christos Spyropoulos (C)

Institute of Energy, Safety and Environmental Technologies, National Center for Scientific Research "Demokritos," Athens, Greece.

Elpida Poulaki (E)

First Department of Pathology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.

Aurelie Prignon (A)

Sorbonne University, UMS28, plateforme LIMP, Laboratoire d'Imagerie Moléculaire Positonique, Hopital Tenon, Paris, France.

Ioannis Kakisis (I)

Vascular Surgery Department, School of Medicine, National and Kapodistrian University of Athens, Attikon Teaching Hospital, Athens, Greece.

Nikolaos G Kostomitsopoulos (NG)

Center of Clinical, Experimental Surgery & Translational Research, Biomedical Research Foundation, Academy of Athens (BRFAA), Athens, Greece.

Penelope Bouziotis (P)

Radiochemical Studies Laboratory, Institute of Nuclear & Radiological Sciences & Technology, Energy & Safety, National Center for Scientific Research "Demokritos," Athens, Greece.

Ioannis V Kostopoulos (IV)

Section of Animal and Human Physiology, Department of Biology, National and Kapodistrian University of Athens, Panepistimiopolis, Ilissia, Athens, Greece.

Ourania Tsitsilonis (O)

Section of Animal and Human Physiology, Department of Biology, National and Kapodistrian University of Athens, Panepistimiopolis, Ilissia, Athens, Greece.

Andreas Lazaris (A)

Vascular Surgery Department, School of Medicine, National and Kapodistrian University of Athens, Attikon Teaching Hospital, Athens, Greece.

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Classifications MeSH