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Induction of heme oxygenase‐1 attenuates cerebral ischemia/reperfusion injury: role of heme
Author(s) -
Volti Giovanni Li,
La Delia Francesco,
Zappalà Agata,
Serapide Maria Francesca,
Puglisi Giovanni,
Cicirata Valentina,
Cicirata Federico
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.733.5
Subject(s) - heme oxygenase , heme , cerebellum , chemistry , brainstem , hippocampus , inducer , bilirubin , biochemistry , pharmacology , medicine , endocrinology , enzyme , biology , gene
We evaluated heme metabolism in different brain regions of transiently ischemized rats (TI). Rats underwent TI for 20 min and following 72h they were sacrificed, brains were dissected and analyzed for heme oxygenase‐1 (HO‐1) distribution. Heme content was determined by HPLC. We firstly assessed the effects of SnCl 2 , an inducer of HO‐1. ELISA showed an increase of HO‐1 protein expression which was followed by increased activity in selected brain regions. We also showed that HO‐1 was induced in neuronal cells of the hippocampus (HP), cerebellum, and brainstem. Increased expression of HO‐1 was also associated to a reduction of heme levels. We evaluated the expression of iNOS, a heme dependent protein. TI strongly increased iNOS expression overall the brain. Pre‐treatment with SnCl 2 decreased both iNOS expression and neuronal cell loss. The effects of SnCl 2 were abolished by SnMP, an inhibitor of HO activity. The results showed that SnCl 2 induces HO‐1 in neuronal cells of selected brain areas, modulates heme metabolism and iNOS expression in TI rats.