To Protect Fatty Livers from Ischemia Reperfusion Injury: Role of Ischemic Postconditioning.


Journal

Digestive diseases and sciences
ISSN: 1573-2568
Titre abrégé: Dig Dis Sci
Pays: United States
ID NLM: 7902782

Informations de publication

Date de publication:
04 2021
Historique:
received: 15 10 2019
accepted: 08 05 2020
pubmed: 27 5 2020
medline: 17 8 2021
entrez: 27 5 2020
Statut: ppublish

Résumé

The benefit of ischemic postconditioning (IPostC) might be the throttled inflow following cold ischemia. The current study investigated advantage and mechanisms of IPostC in healthy and fatty rat livers. Male SD rats received a high-fat diet to induce fatty livers. Isolated liver perfusion was performed after 24 h ischemia at 4 °C as well as in vivo experiments after 90 min warm ischemia. The so-called follow-up perfusions served to investigate the hypothesis that medium from IPostC experiments is less harmful. Lactate dehydrogenase (LDH), transaminases, different cytokines, and gene expressions, respectively, were measured. Fatty livers showed histologically mild inflammation and moderate to severe fat storage. IPostC reduced LDH and TXB IPostC showed protective effects after ischemia in situ and in vivo in healthy and fatty livers. Restricted cyclic inflow was an important mechanism and further suggested involvement of necroptosis. IPostC represents a promising and easy intervention to improve outcomes after transplantation.

Sections du résumé

BACKGROUND
The benefit of ischemic postconditioning (IPostC) might be the throttled inflow following cold ischemia. The current study investigated advantage and mechanisms of IPostC in healthy and fatty rat livers.
METHODS
Male SD rats received a high-fat diet to induce fatty livers. Isolated liver perfusion was performed after 24 h ischemia at 4 °C as well as in vivo experiments after 90 min warm ischemia. The so-called follow-up perfusions served to investigate the hypothesis that medium from IPostC experiments is less harmful. Lactate dehydrogenase (LDH), transaminases, different cytokines, and gene expressions, respectively, were measured.
RESULTS
Fatty livers showed histologically mild inflammation and moderate to severe fat storage. IPostC reduced LDH and TXB
CONCLUSIONS
IPostC showed protective effects after ischemia in situ and in vivo in healthy and fatty livers. Restricted cyclic inflow was an important mechanism and further suggested involvement of necroptosis. IPostC represents a promising and easy intervention to improve outcomes after transplantation.

Identifiants

pubmed: 32451758
doi: 10.1007/s10620-020-06328-w
pii: 10.1007/s10620-020-06328-w
pmc: PMC7990852
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1349-1359

Subventions

Organisme : Deutsche Forschungsgemeinschaft
ID : DFG STE 1022/2-3
Organisme : Deutsche Forschungsgemeinschaft
ID : DFG STE 1022/4-1

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Auteurs

Julia Schewe (J)

Berlin Institute of Health, Charité - Universitätsmedizin Berlin, Berlin, Germany.

Marie-Christine Makeschin (MC)

Department of Pathology, University Hospital, LMU Munich, Munich, Germany.

Andrej Khandoga (A)

Department of Surgery, University Hospital, LMU Munich, Munich, Germany.

Jiang Zhang (J)

Department of Medicine II, University Hospital, Liver Centre Munich, LMU Munich, Campus Grosshadern, Marchioninistrasse 15, 81377, Munich, Germany.

Doris Mayr (D)

Department of Pathology, University Hospital, LMU Munich, Munich, Germany.

Simon Rothenfußer (S)

Division of Clinical Pharmacology, University Hospital, LMU Munich, Munich, Germany.

Max Schnurr (M)

Division of Clinical Pharmacology, University Hospital, LMU Munich, Munich, Germany.

Alexander L Gerbes (AL)

Department of Medicine II, University Hospital, Liver Centre Munich, LMU Munich, Campus Grosshadern, Marchioninistrasse 15, 81377, Munich, Germany.

Christian J Steib (CJ)

Department of Medicine II, University Hospital, Liver Centre Munich, LMU Munich, Campus Grosshadern, Marchioninistrasse 15, 81377, Munich, Germany. christian.steib@med.uni-muenchen.de.

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