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Cross-talk between hydrogen sulfide and carbon monoxide in the mechanism of experimental gastric ulcers healing, regulation of gastric blood flow and accompanying inflammation.
Biochem Pharmacol. 2018 03; 149:131-142.BP

Abstract

Hydrogen sulfide (H2S) and carbon monoxide (CO) exert gastroprotection against acute gastric lesions. We determined the cross-talk between H2S and CO in gastric ulcer healing process and regulation of gastric blood flow (GBF) at ulcer margin. Male Wistar rats with acetic acid-induced gastric ulcers were treated i.g. throughout 9 days with vehicle (control), NaHS (0.1-10 mg/kg) +/- zinc protoporphyrin (ZnPP, 10 mg/kg), d,l-propargylglycine (PAG, 30 mg/kg), CO-releasing CORM-2 (2.5 mg/kg) +/- PAG. GBF was assessed by laser flowmetry, ulcer area was determined by planimetry/histology. Gastric mucosal H2S production was analysed spectrophotometrically. Protein and/or mRNA expression at ulcer margin for vascular endothelial growth factor (VEGF)A, epidermal growth factor receptor (EGFr), cystathionine-γ-lyase (CSE), cystathionine-β-synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3-MST), heme oxygenases (HOs), nuclear factor (erythroid-derived 2)-like 2 (Nrf-2), cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS), IL-1β, TNF-α and hypoxia inducible factor (HIF)-1α were determined by real-time PCR or western blot. IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, IL-13, IFN-γ, TNF-α, GM-CSF plasma concentration was assessed using Luminex platform. NaHS dose-dependently decreased ulcer area and increased GBF but ZnPP attenuated these effects. PAG decreased H2S production but failed to affect CORM-2-mediated ulcer healing and vasodilation. NaHS increased Nrf-2, EGFr, VEGFA and decreased pro-inflammatory markers expression and IL-1β, IL-2, IL-13, TNF-α, GM-CSF plasma concentration. CORM-2 decreased IL-1β and GM-CSF plasma levels. We conclude that NaHS accelerates gastric ulcer healing increasing microcirculation and Nrf-2, EGFr, VEGFA expression. H2S-mediated ulcer healing involves endogenous CO activity while CO does not require H2S. NaHS decreases systemic inflammation more effectively than CORM-2.

Authors+Show Affiliations

Department of Physiology, Jagiellonian University Medical College, 16 Grzegorzecka Street 31-531 Cracow, Poland. Electronic address: m.magierowski@uj.edu.pl.Department of Physiology, Jagiellonian University Medical College, 16 Grzegorzecka Street 31-531 Cracow, Poland.Department of Physiology, Jagiellonian University Medical College, 16 Grzegorzecka Street 31-531 Cracow, Poland.Department of Physiology, Jagiellonian University Medical College, 16 Grzegorzecka Street 31-531 Cracow, Poland.Department of Physiology, Jagiellonian University Medical College, 16 Grzegorzecka Street 31-531 Cracow, Poland.Department of Physiology, Jagiellonian University Medical College, 16 Grzegorzecka Street 31-531 Cracow, Poland.Department of Physiology, Jagiellonian University Medical College, 16 Grzegorzecka Street 31-531 Cracow, Poland.Department of Physiology, Jagiellonian University Medical College, 16 Grzegorzecka Street 31-531 Cracow, Poland.Department of Physiology, Jagiellonian University Medical College, 16 Grzegorzecka Street 31-531 Cracow, Poland.

Pub Type(s)

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

Language

eng

PubMed ID

29203367

Citation

Magierowski, Marcin, et al. "Cross-talk Between Hydrogen Sulfide and Carbon Monoxide in the Mechanism of Experimental Gastric Ulcers Healing, Regulation of Gastric Blood Flow and Accompanying Inflammation." Biochemical Pharmacology, vol. 149, 2018, pp. 131-142.
Magierowski M, Magierowska K, Hubalewska-Mazgaj M, et al. Cross-talk between hydrogen sulfide and carbon monoxide in the mechanism of experimental gastric ulcers healing, regulation of gastric blood flow and accompanying inflammation. Biochem Pharmacol. 2018;149:131-142.
Magierowski, M., Magierowska, K., Hubalewska-Mazgaj, M., Surmiak, M., Sliwowski, Z., Wierdak, M., Kwiecien, S., Chmura, A., & Brzozowski, T. (2018). Cross-talk between hydrogen sulfide and carbon monoxide in the mechanism of experimental gastric ulcers healing, regulation of gastric blood flow and accompanying inflammation. Biochemical Pharmacology, 149, 131-142. https://doi.org/10.1016/j.bcp.2017.11.020
Magierowski M, et al. Cross-talk Between Hydrogen Sulfide and Carbon Monoxide in the Mechanism of Experimental Gastric Ulcers Healing, Regulation of Gastric Blood Flow and Accompanying Inflammation. Biochem Pharmacol. 2018;149:131-142. PubMed PMID: 29203367.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cross-talk between hydrogen sulfide and carbon monoxide in the mechanism of experimental gastric ulcers healing, regulation of gastric blood flow and accompanying inflammation. AU - Magierowski,Marcin, AU - Magierowska,Katarzyna, AU - Hubalewska-Mazgaj,Magdalena, AU - Surmiak,Marcin, AU - Sliwowski,Zbigniew, AU - Wierdak,Mateusz, AU - Kwiecien,Slawomir, AU - Chmura,Anna, AU - Brzozowski,Tomasz, Y1 - 2017/12/01/ PY - 2017/09/30/received PY - 2017/11/29/accepted PY - 2017/12/6/pubmed PY - 2018/12/12/medline PY - 2017/12/6/entrez KW - Carbon monoxide KW - Gastric blood flow KW - Gastric ulcer healing KW - Hydrogen sulfide KW - Inflammation SP - 131 EP - 142 JF - Biochemical pharmacology JO - Biochem Pharmacol VL - 149 N2 - Hydrogen sulfide (H2S) and carbon monoxide (CO) exert gastroprotection against acute gastric lesions. We determined the cross-talk between H2S and CO in gastric ulcer healing process and regulation of gastric blood flow (GBF) at ulcer margin. Male Wistar rats with acetic acid-induced gastric ulcers were treated i.g. throughout 9 days with vehicle (control), NaHS (0.1-10 mg/kg) +/- zinc protoporphyrin (ZnPP, 10 mg/kg), d,l-propargylglycine (PAG, 30 mg/kg), CO-releasing CORM-2 (2.5 mg/kg) +/- PAG. GBF was assessed by laser flowmetry, ulcer area was determined by planimetry/histology. Gastric mucosal H2S production was analysed spectrophotometrically. Protein and/or mRNA expression at ulcer margin for vascular endothelial growth factor (VEGF)A, epidermal growth factor receptor (EGFr), cystathionine-γ-lyase (CSE), cystathionine-β-synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3-MST), heme oxygenases (HOs), nuclear factor (erythroid-derived 2)-like 2 (Nrf-2), cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS), IL-1β, TNF-α and hypoxia inducible factor (HIF)-1α were determined by real-time PCR or western blot. IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, IL-13, IFN-γ, TNF-α, GM-CSF plasma concentration was assessed using Luminex platform. NaHS dose-dependently decreased ulcer area and increased GBF but ZnPP attenuated these effects. PAG decreased H2S production but failed to affect CORM-2-mediated ulcer healing and vasodilation. NaHS increased Nrf-2, EGFr, VEGFA and decreased pro-inflammatory markers expression and IL-1β, IL-2, IL-13, TNF-α, GM-CSF plasma concentration. CORM-2 decreased IL-1β and GM-CSF plasma levels. We conclude that NaHS accelerates gastric ulcer healing increasing microcirculation and Nrf-2, EGFr, VEGFA expression. H2S-mediated ulcer healing involves endogenous CO activity while CO does not require H2S. NaHS decreases systemic inflammation more effectively than CORM-2. SN - 1873-2968 UR - https://www.unboundmedicine.com/medline/citation/29203367/Cross_talk_between_hydrogen_sulfide_and_carbon_monoxide_in_the_mechanism_of_experimental_gastric_ulcers_healing_regulation_of_gastric_blood_flow_and_accompanying_inflammation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-2952(17)30701-3 DB - PRIME DP - Unbound Medicine ER -