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Int. J. Mol. Sci. 2016, 17(4), 442; doi:10.3390/ijms17040442

The Protective Role of Carbon Monoxide (CO) Produced by Heme Oxygenases and Derived from the CO-Releasing Molecule CORM-2 in the Pathogenesis of Stress-Induced Gastric Lesions: Evidence for Non-Involvement of Nitric Oxide (NO)

1
Department of Physiology, Jagiellonian University Medical College, 31-531 Cracow, Poland
2
Division of Molecular Biology and Clinical Genetics, Department of Medicine, Jagiellonian University Medical College, 31-006 Cracow, Poland
3
Department of Forensic Toxicology, Institute of Forensic Research, 31-033 Cracow, Poland
4
Department of Ergonomics and Exercise Physiology, Faculty of Health Sciences, Jagiellonian University Medical College, 31-531 Cracow, Poland
*
Author to whom correspondence should be addressed.
Academic Editor: Masatoshi Maki
Received: 24 January 2016 / Revised: 18 March 2016 / Accepted: 18 March 2016 / Published: 24 March 2016
(This article belongs to the Special Issue Metalloproteins)
View Full-Text   |   Download PDF [9440 KB, uploaded 24 March 2016]   |  

Abstract

Carbon monoxide (CO) produced by heme oxygenase (HO)-1 and HO-2 or released from the CO-donor, tricarbonyldichlororuthenium (II) dimer (CORM-2) causes vasodilation, with unknown efficacy against stress-induced gastric lesions. We studied whether pretreatment with CORM-2 (0.1–10 mg/kg oral gavage (i.g.)), RuCl3 (1 mg/kg i.g.), zinc protoporphyrin IX (ZnPP) (10 mg/kg intraperitoneally (i.p.)), hemin (1–10 mg/kg i.g.) and CORM-2 (1 mg/kg i.g.) combined with NG-nitro-l-arginine (l-NNA, 20 mg/kg i.p.), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 10 mg/kg i.p.), indomethacin (5 mg/kg i.p.), SC-560 (5 mg/kg i.g.), and celecoxib (10 mg/kg i.g.) affects gastric lesions following 3.5 h of water immersion and restraint stress (WRS). Gastric blood flow (GBF), the number of gastric lesions and gastric CO and nitric oxide (NO) contents, blood carboxyhemoglobin (COHb) level and the gastric expression of HO-1, HO-2, hypoxia inducible factor 1α (HIF-1α), tumor necrosis factor α (TNF-α), cyclooxygenase (COX)-2 and inducible NO synthase (iNOS) were determined. CORM-2 (1 mg/kg i.g.) and hemin (10 mg/kg i.g.) significantly decreased WRS lesions while increasing GBF, however, RuCl3 was ineffective. The impact of CORM-2 was reversed by ZnPP, ODQ, indomethacin, SC-560 and celecoxib, but not by l-NNA. CORM-2 decreased NO and increased HO-1 expression and CO and COHb content, downregulated HIF-1α, as well as WRS-elevated COX-2 and iNOS mRNAs. Gastroprotection by CORM-2 and HO depends upon CO’s hyperemic and anti-inflammatory properties, but is independent of NO. View Full-Text
Keywords: carbon monoxide; stress; nitric oxide; gastroprotection; gastric blood flow; heme oxygenase-1; cyclooxygenases; soluble guanylyl cyclase; hypoxia inducible factor 1α carbon monoxide; stress; nitric oxide; gastroprotection; gastric blood flow; heme oxygenase-1; cyclooxygenases; soluble guanylyl cyclase; hypoxia inducible factor 1α
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Magierowska, K.; Magierowski, M.; Surmiak, M.; Adamski, J.; Mazur-Bialy, A.I.; Pajdo, R.; Sliwowski, Z.; Kwiecien, S.; Brzozowski, T. The Protective Role of Carbon Monoxide (CO) Produced by Heme Oxygenases and Derived from the CO-Releasing Molecule CORM-2 in the Pathogenesis of Stress-Induced Gastric Lesions: Evidence for Non-Involvement of Nitric Oxide (NO). Int. J. Mol. Sci. 2016, 17, 442.

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