Resveratrol therapy improves liver function via estrogen-receptors after hemorrhagic shock in rats.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2022
Historique:
received: 13 02 2022
accepted: 20 09 2022
entrez: 13 10 2022
pubmed: 14 10 2022
medline: 18 10 2022
Statut: epublish

Résumé

Resveratrol may improve organ dysfunction after experimental hemorrhagic or septic shock, and some of these effects appear to be mediated by estrogen receptors. However, the influence of resveratrol on liver function and hepatic microcirculation after hemorrhagic shock is unknown, and a presumed mediation via estrogen receptors has not been investigated in this context. Male Sprague-Dawley rats (200-300g, n = 14/group) underwent hemorrhagic shock for 90 min (MAP 35±5 mmHg) and were resuscitated with shed blood and Ringer's solution. Animals were treated intravenously with vehicle (1% EtOH), resveratrol (0.2 mg/kg), the unselective estrogen receptor antagonist ICI 182,780 (0.05 mg/kg) or resveratrol + ICI 182,780 prior to retransfusion. Sham-operated animals did not undergo hemorrhage but were treated likewise. After 2 hours of reperfusion, liver function was assessed either by plasma disappearance rate of indocyanine green (PDRICG) or evaluation of hepatic perfusion and hepatic integrity by intravital microscopy, serum enzyme as well as cytokine levels. Compared to vehicle controls, administration of resveratrol significantly improved PDRICG, hepatic perfusion index and hepatic integrity after hemorrhagic shock. The co-administration of ICI 182,780 completely abolished the protective effect only with regard to liver function. This study shows that resveratrol may improve liver function and hepatocellular integrity after hemorrhagic shock in rats; estrogen receptors mediate these effects at least partially.

Sections du résumé

BACKGROUND
Resveratrol may improve organ dysfunction after experimental hemorrhagic or septic shock, and some of these effects appear to be mediated by estrogen receptors. However, the influence of resveratrol on liver function and hepatic microcirculation after hemorrhagic shock is unknown, and a presumed mediation via estrogen receptors has not been investigated in this context.
METHODS
Male Sprague-Dawley rats (200-300g, n = 14/group) underwent hemorrhagic shock for 90 min (MAP 35±5 mmHg) and were resuscitated with shed blood and Ringer's solution. Animals were treated intravenously with vehicle (1% EtOH), resveratrol (0.2 mg/kg), the unselective estrogen receptor antagonist ICI 182,780 (0.05 mg/kg) or resveratrol + ICI 182,780 prior to retransfusion. Sham-operated animals did not undergo hemorrhage but were treated likewise. After 2 hours of reperfusion, liver function was assessed either by plasma disappearance rate of indocyanine green (PDRICG) or evaluation of hepatic perfusion and hepatic integrity by intravital microscopy, serum enzyme as well as cytokine levels.
RESULTS
Compared to vehicle controls, administration of resveratrol significantly improved PDRICG, hepatic perfusion index and hepatic integrity after hemorrhagic shock. The co-administration of ICI 182,780 completely abolished the protective effect only with regard to liver function.
CONCLUSIONS
This study shows that resveratrol may improve liver function and hepatocellular integrity after hemorrhagic shock in rats; estrogen receptors mediate these effects at least partially.

Identifiants

pubmed: 36227865
doi: 10.1371/journal.pone.0275632
pii: PONE-D-22-04404
pmc: PMC9560221
doi:

Substances chimiques

Cytokines 0
Estrogen Receptor Antagonists 0
Estrogens 0
Receptors, Estrogen 0
Fulvestrant 22X328QOC4
Ringer's Solution 8026-10-6
Indocyanine Green IX6J1063HV
Resveratrol Q369O8926L

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0275632

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Alexander Wolf (A)

Department of Anesthesiology, Critical Care and Pain Medicine, Universitätsklinikum Knappschaftskrankenhaus Bochum GmbH, Bochum, Germany.

Tobias Fink (T)

Department of Anesthesiology, Critical Care and Pain Therapy, Saarland University Hospital, Homburg (Saar), Germany.

Jochen Hinkelbein (J)

Department of Anesthesiology and Intensive Care Medicine, University Hospital and Medical Faculty, University Hospital Cologne, Cologne, Germany.

Thilo Mertke (T)

Department of Anesthesiology, Critical Care and Pain Therapy, Saarland University Hospital, Homburg (Saar), Germany.

Thomas Volk (T)

Department of Anesthesiology, Critical Care and Pain Therapy, Saarland University Hospital, Homburg (Saar), Germany.

Alexander Mathes (A)

Department of Anesthesiology and Intensive Care Medicine, University Hospital and Medical Faculty, University Hospital Cologne, Cologne, Germany.

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Classifications MeSH