Carbon monoxide released from its pharmacological donor, tricarbonyldichlororuthenium (II) dimer, accelerates the healing of pre-existing gastric ulcers.

Marcin MagierowskiKatarzyna MagierowskaMagdalena Hubalewska-MazgajZbigniew SliwowskiGrzegorz GinterRobert PajdoAnna ChmuraSlawomir KwiecienTomasz Brzozowski

Published in: British journal of pharmacology (2017)

CO released from CORM-2 or endogenously produced by the HO1/Nrf2 pathway accelerates gastric ulcer healing via an increase in GBF, an up-regulation in EGF expression and down-regulation of the inflammatory response.

Keyphrases

inflammatory response
poor prognosis
oxidative stress
lipopolysaccharide induced
growth factor
cell proliferation