Oxidative gastric mucosal damage induced by ischemia/reperfusion and the mechanisms of its prevention by carbon monoxide-releasing tricarbonyldichlororuthenium (II) dimer.
Animals
Carbon Monoxide
/ metabolism
Disease Models, Animal
Gasotransmitters
/ pharmacology
Gastric Mucosa
/ drug effects
Heme Oxygenase (Decyclizing)
/ metabolism
Humans
Hydrogen Sulfide
/ metabolism
Male
Nitric Oxide
/ metabolism
Organometallic Compounds
/ pharmacology
Oxidative Stress
/ drug effects
Rats
Reperfusion Injury
/ complications
Carbon monoxide
DNA oxidation
Gastric mucosa
Ischemia/reperfusion
Journal
Free radical biology & medicine
ISSN: 1873-4596
Titre abrégé: Free Radic Biol Med
Pays: United States
ID NLM: 8709159
Informations de publication
Date de publication:
12 2019
12 2019
Historique:
received:
15
07
2019
revised:
25
09
2019
accepted:
26
09
2019
pubmed:
1
10
2019
medline:
4
9
2020
entrez:
1
10
2019
Statut:
ppublish
Résumé
Endogenous gaseous mediators, such as nitric oxide, hydrogen sulfide or carbon monoxide (CO) are known to exert anti-inflammatory and anti-oxidative activity due to modulation of various molecular pahtways. Therefore, we aimed to investigate if CO released from tricarbonyldichlororuthenium (II) dimer (CORM-2) prevents gastric mucosa against ischemia/reperfusion (I/R)-induced injury in male Wistar rats. Animals were pretreated i.g. With vehicle (DMSO and saline, 1:10), CORM-2 (1, 5 or 10 mg/kg) or zinc protoporphyrin IX (ZnPP, 10 mg/kg i.p.), the HMOXs inhibitor. In separate series, rats were pretreated with CORM-2 (5 mg/kg) applied in combination with glibenclamide (10 mg/kg i.g.), N
Identifiants
pubmed: 31568823
pii: S0891-5849(19)31177-3
doi: 10.1016/j.freeradbiomed.2019.09.032
pii:
doi:
Substances chimiques
Gasotransmitters
0
Organometallic Compounds
0
tricarbonyldichlororuthenium (II) dimer
0
Nitric Oxide
31C4KY9ESH
Carbon Monoxide
7U1EE4V452
Heme Oxygenase (Decyclizing)
EC 1.14.14.18
Hydrogen Sulfide
YY9FVM7NSN
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
198-208Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.