6533b837fe1ef96bd12a1ec8
RESEARCH PRODUCT
Participation of Heme Oxygenase-1 in a Model of Acute Inflammation
María Isabel GuillínMaría Josí AlcarazAna María Vicentesubject
0301 basic medicinemedicine.medical_specialtyNitric Oxide Synthase Type IIInflammationGeneral Biochemistry Genetics and Molecular BiologyNitric oxideMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicinemedicineAnimalsProstaglandin E2HemeInflammationbiologyZymosanZymosanMembrane ProteinsIsoenzymesHeme oxygenaseDisease Models Animal030104 developmental biologyEndocrinologychemistryCyclooxygenase 2Prostaglandin-Endoperoxide Synthases030220 oncology & carcinogenesisHeme Oxygenase (Decyclizing)ImmunologyMacrophages Peritonealbiology.proteinHeminFemaleCyclooxygenaseNitric Oxide Synthasemedicine.symptomHeme Oxygenase-1medicine.drugHemindescription
In this study, the role of heme oxygenase-1 (HO-1) in the inflammatory response elicited by zymosan in the mouse air pouch model has been examined. This response is characterized by a time-dependent increase in HO-1 expression in the leukocytes migrating into the exudates. At 24–48 h maximal HO-1 expression was accompanied by reduced cyclooxygenase-2 (COX-2) and nitric oxide synthase-2 (NOS-2) expression as well as low levels of inflammatory mediators. Hemin administration into the air pouch caused an elevation of HO-1 protein and bilirubin levels induced by zymosan with inhibition of COX-2 expression. In mouse peritoneal macrophages from hemin-injected mice, we also observed an increased expression of HO-1 with inhibition of COX-2 expression and prostaglandin E2 (PGE2) levels. Our data suggest an anti-inflammatory role for HO-1 in the response induced by this phagocytic stimulus.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2003-04-24 | Experimental Biology and Medicine |