ArticlePloS one2015
Carbon Monoxide (CO) Released from Tricarbonyldichlororuthenium (II) Dimer (CORM-2) in Gastroprotection against Experimental Ethanol-Induced Gastric Damage.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 46 citations in OpenAlex.
- Transcriptomic Identification of Diagnostic Biomarkers for Alcohol-Associated Liver Cirrhosis: Integration of Population-Level Epidemiology with Multi-Cohort Transcriptomic Analysis.International journal of molecular sciences · 2026Article
- Synergistic interactions of ruthenium-based carbon monoxide-releasing molecules and antibiotics in their effects onMicrobiology (Reading, England) · 2026Article
- Carbon monoxide (CO) derived from the CO-releasing molecule CORM-2 reduces peritoneal adhesion formation in a rat model.Molecular biology reports · 2023Article
- Novel Toxicodynamic Model of Subcutaneous Envenomation to Characterize Snake Venom Coagulopathies and Assess the Efficacy of Site-Directed Inorganic Antivenoms.International journal of molecular sciences · 2023Article
- Reassessing CORM-A1: redox chemistry and idiosyncratic CO-releasing characteristics of the widely used carbon monoxide donor.Chemical science · 2023Article
- Carbon monoxide signaling and soluble guanylyl cyclase: Facts, myths, and intriguing possibilities.Biochemical pharmacology · 2022Review
- Article
- "CO in a pill": Towards oral delivery of carbon monoxide for therapeutic applications.Journal of controlled release : official journal of the Controlled Release Society · 2021Review
- Malvidin Protects against and Repairs Peptic Ulcers in Mice by Alleviating Oxidative Stress and Inflammation.Nutrients · 2021Article
- Organic carbon monoxide prodrug, BW-CO-111, in protection against chemically-induced gastric mucosal damage.Acta pharmaceutica Sinica. B · 2021Article
- Article
- CO-Releasing Molecule-2 Induces Nrf2/ARE-Dependent Heme Oxygenase-1 Expression Suppressing TNF-α-Induced Pulmonary Inflammation.Journal of clinical medicine · 2019Article
- Alterations in Gastric Mucosal Expression of Calcitonin Gene-Related Peptides, Vanilloid Receptors, and Heme Oxygenase-1 Mediate Gastroprotective Action of Carbon Monoxide against Ethanol-Induced Gastric Mucosal Lesions.International journal of molecular sciences · 2018Article
- Mechanisms of curcumin-induced gastroprotection against ethanol-induced gastric mucosal lesions.Journal of gastroenterology · 2018Article
- Arachidonic Acid Induces ARE/Nrf2-Dependent Heme Oxygenase-1 Transcription in Rat Brain Astrocytes.Molecular neurobiology · 2018Article
- Gastroprotective Effects of Sulphated Polysaccharides from the Alga Caulerpa mexicana Reducing Ethanol-Induced Gastric Damage.Pharmaceuticals (Basel, Switzerland) · 2018Article
- An Overview of the Potential Therapeutic Applications of CO-Releasing Molecules.Bioinorganic chemistry and applications · 2018Review
- Nitric oxide, afferent sensory nerves, and antioxidative enzymes in the mechanism of protection mediated by tricarbonyldichlororuthenium(II) dimer and sodium hydrosulfide against aspirin-induced gastric damage.Journal of gastroenterology · 2018Article
- Carbon monoxide released from its pharmacological donor, tricarbonyldichlororuthenium (II) dimer, accelerates the healing of pre-existing gastric ulcers.British journal of pharmacology · 2017Article
- Gaseous Mediators in Gastrointestinal Mucosal Defense and Injury.Digestive diseases and sciences · 2017Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The physiological gaseous molecule, carbon monoxide (CO) becomes a subject of extensive investigation due to its vasoactive activity throughout the body but its role in gastroprotection has been little investigated. We determined the mechanism of CO released from its donor tricarbonyldichlororuthenium (II) dimer (CORM-2) in protection of gastric mucosa against 75% ethanol-induced injury. Rats were pretreated with CORM-2 30 min prior to 75% ethanol with or without 1) non-selective (indomethacin) or selective cyclooxygenase (COX)-1 (SC-560) and COX-2 (celecoxib) inhibitors, 2) nitric oxide (NO) synthase inhibitor L-NNA, 3) ODQ, a soluble guanylyl cyclase (sGC) inhibitor, hemin, a heme oxygenase (HO)-1 inductor or zinc protoporphyrin IX (ZnPPIX), an inhibitor of HO-1 activity. The CO content in gastric mucosa and carboxyhemoglobin (COHb) level in blood was analyzed by gas chromatography. The gastric mucosal mRNA expression for HO-1, COX-1, COX-2, iNOS, IL-4, IL-1β was analyzed by real-time PCR while HO-1, HO-2 and Nrf2 protein expression was determined by Western Blot. Pretreatment with CORM-2 (0.5-10 mg/kg) dose-dependently attenuated ethanol-induced lesions and raised gastric blood flow (GBF) but large dose of 100 mg/kg was ineffective. CORM-2 (5 mg/kg and 50 mg/kg i.g.) significantly increased gastric mucosal CO content and whole blood COHb level. CORM-2-induced protection was reversed by indomethacin, SC-560 and significantly attenuated by celecoxib, ODQ and L-NNA. Hemin significantly reduced ethanol damage and raised GBF while ZnPPIX which exacerbated ethanol-induced injury inhibited CORM-2- and hemin-induced gastroprotection and the accompanying rise in GBF. CORM-2 significantly increased gastric mucosal HO-1 mRNA expression and decreased mRNA expression for iNOS, IL-1β, COX-1 and COX-2 but failed to affect HO-1 and Nrf2 protein expression decreased by ethanol. We conclude that CORM-2 released CO exerts gastroprotection against ethanol-induced gastric lesions involving an increase in gastric microcirculation mediated by sGC/cGMP, prostaglandins derived from COX-1, NO-NOS system and its anti-inflammatory properties.
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