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The Role of Haem Oxygenase‐1 in the Decrease of Endothelial Intercellular Adhesion Molecule‐1 Expression by Curcumin
Author(s) -
Olszanecki Rafal,
Gebska Anna,
Korbut Ryszard
Publication year - 2007
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2007.00151.x
Subject(s) - curcumin , lipopolysaccharide , in vivo , heme oxygenase , pharmacology , in vitro , icam 1 , cell adhesion molecule , chemistry , intracellular , intercellular adhesion molecule 1 , myeloperoxidase , tumor necrosis factor alpha , endothelium , heme , inflammation , biochemistry , biology , immunology , enzyme , endocrinology , microbiology and biotechnology
Intercellular adhesion molecule‐1 (ICAM‐1) is involved in neutrophil transmigration across endothelium during sepsis‐induced acute lung injury and anti‐ICAM‐1 interventions may represent new strategy of pulmonary protection. Haem oxygenase‐1 (HO‐1) has been demonstrated to exert anti‐inflammatory actions via decrease of expression of adhesion molecules. We investigated the role of HO‐1 in the action of curcumin, a naturally occurring yellow pigment isolated from plant Curcuma longa L., on ICAM‐1 expression in tumour necrosis factor‐α‐stimulated EA.hy926 cells and lungs of lipopolysaccharide‐treated mice. Both, in vitro and in vivo curcumin induced HO‐1 and curcumin‐elicited induction of HO‐1 was associated with inhibition ICAM‐1 expression. Moreover, curcumin significantly inhibited pulmonary sequestration of leucocytes in response to lipopolysaccharide as evidenced by decrease of myeloperoxidase activity in lung tissue. Both in vitro and in vivo effects of curcumin were reversed by an inhibitor of HO activity, chromium (III) mesoporphyrin IX chloride. We conclude that induction of HO‐1, via decrease of endothelial ICAM‐1, plays a pivotal role in curcumin‐dependent prevention of pulmonary sequestration of neutrophils in a mouse model of endotoxaemia.