Sevoflurane postconditioning is not mediated by ferritin accumulation and cannot be rescued by simvastatin in isolated streptozotocin-induced diabetic rat hearts.
Animals
Diabetes Mellitus, Experimental
/ complications
Disease Models, Animal
Ferritins
/ genetics
Gene Expression Regulation
/ drug effects
Heart
/ drug effects
Iron
Ischemic Preconditioning, Myocardial
Male
Myocardial Infarction
/ genetics
Nitric Oxide
/ metabolism
Rats
Sevoflurane
/ administration & dosage
Simvastatin
/ pharmacology
Streptozocin
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2019
2019
Historique:
received:
08
10
2018
accepted:
09
01
2019
entrez:
26
1
2019
pubmed:
27
1
2019
medline:
29
10
2019
Statut:
epublish
Résumé
Sevoflurane postconditioning (sevo postC) is an attractive and amenable approach that can protect the myocardium against ischemia/reperfusion (I/R)-injury. Unlike ischemic preconditioning (IPC), sevo postC does not require additional induced ischemic periods to a heart that is already at risk. IPC was previously shown to generate myocardial protection against I/R-injury through regulation of iron homeostasis and de novo ferritin synthesis, a process found to be impaired in the diabetic state. The current study investigated whether alterations in iron homeostasis and ferritin mRNA and protein accumulation are also involved in the cardioprotective effects generated by sevo postC. It was also investigated whether the protective effects of sevo postC in the diabetic state can be salvaged by simvastatin, through inducing nitric oxide (NO) bioavailability/activity, in isolated streptozotocin (STZ)-induced diabetic hearts (DH). Isolated rat hearts from healthy Controls and diabetic animals were retrogradely perfused using the Langendorff configuration and subjected to prolonged ischemia and reperfusion, with and without (2.4 and 3.6%) sevo postC and/or pre-treatment with simvastatin (0.5 mg/kg). Sevo postC significantly reduced infarct size and improved myocardial function in healthy Controls but not in isolated DH. The sevo postC mediated myocardial protection against I/R-injury was not associated with de novo ferrtin synthesis. Furthermore, simvastatin aggravated myocardial injury after sevo postC in STZ-induced DHs, likely due to increasing NO levels. Despite the known mechanistic overlaps between PC and postC stimuli, distinct differences underlie the cardioprotective interventions against myocardial I/R-injury and are impaired in the DH. Sevo postC mediated cardioprotection, unlike IPC, does not involve de novo ferritin accumulation and cannot be rescued by simvastatin in STZ-induced DHs.
Identifiants
pubmed: 30682140
doi: 10.1371/journal.pone.0211238
pii: PONE-D-18-29187
pmc: PMC6347357
doi:
Substances chimiques
Nitric Oxide
31C4KY9ESH
Sevoflurane
38LVP0K73A
Streptozocin
5W494URQ81
Ferritins
9007-73-2
Simvastatin
AGG2FN16EV
Iron
E1UOL152H7
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0211238Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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