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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 Mar 24; 17(4):442.IJ

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 N(G)-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.

Authors+Show Affiliations

Department of Physiology, Jagiellonian University Medical College, 31-531 Cracow, Poland. k.jasnos@interia.pl.Department of Physiology, Jagiellonian University Medical College, 31-531 Cracow, Poland. m.magierowski@uj.edu.pl.Department of Physiology, Jagiellonian University Medical College, 31-531 Cracow, Poland. marcin.surmiak@uj.edu.pl. Division of Molecular Biology and Clinical Genetics, Department of Medicine, Jagiellonian University Medical College, 31-006 Cracow, Poland. marcin.surmiak@uj.edu.pl.Department of Forensic Toxicology, Institute of Forensic Research, 31-033 Cracow, Poland. juliusz.adamski@gmail.com.Department of Ergonomics and Exercise Physiology, Faculty of Health Sciences, Jagiellonian University Medical College, 31-531 Cracow, Poland. agnieszka.mazur@uj.edu.pl.Department of Physiology, Jagiellonian University Medical College, 31-531 Cracow, Poland. mppajdo@cyf-kr.edu.pl.Department of Physiology, Jagiellonian University Medical College, 31-531 Cracow, Poland. agazs@poczta.fm.Department of Physiology, Jagiellonian University Medical College, 31-531 Cracow, Poland. skwiecien@cm-uj.krakow.pl.Department of Physiology, Jagiellonian University Medical College, 31-531 Cracow, Poland. mpbrzozo@cyf-kr.edu.pl.

Pub Type(s)

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

Language

eng

PubMed ID

27023525

Citation

Magierowska, Katarzyna, et al. "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)." International Journal of Molecular Sciences, vol. 17, no. 4, 2016, p. 442.
Magierowska K, Magierowski M, Surmiak M, et al. 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(4):442.
Magierowska, K., Magierowski, M., Surmiak, M., Adamski, J., Mazur-Bialy, A. I., Pajdo, R., Sliwowski, Z., Kwiecien, S., & Brzozowski, T. (2016). 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). International Journal of Molecular Sciences, 17(4), 442. https://doi.org/10.3390/ijms17040442
Magierowska K, et al. 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 Mar 24;17(4):442. PubMed PMID: 27023525.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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). AU - Magierowska,Katarzyna, AU - Magierowski,Marcin, AU - Surmiak,Marcin, AU - Adamski,Juliusz, AU - Mazur-Bialy,Agnieszka Irena, AU - Pajdo,Robert, AU - Sliwowski,Zbigniew, AU - Kwiecien,Slawomir, AU - Brzozowski,Tomasz, Y1 - 2016/03/24/ PY - 2016/01/24/received PY - 2016/03/18/revised PY - 2016/03/18/accepted PY - 2016/3/30/entrez PY - 2016/3/31/pubmed PY - 2016/12/15/medline KW - carbon monoxide KW - cyclooxygenases KW - gastric blood flow KW - gastroprotection KW - heme oxygenase-1 KW - hypoxia inducible factor 1α KW - nitric oxide KW - soluble guanylyl cyclase KW - stress SP - 442 EP - 442 JF - International journal of molecular sciences JO - Int J Mol Sci VL - 17 IS - 4 N2 - 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 N(G)-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. SN - 1422-0067 UR - https://www.unboundmedicine.com/medline/citation/27023525/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__ L2 - https://www.mdpi.com/resolver?pii=ijms17040442 DB - PRIME DP - Unbound Medicine ER -