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Role of cyclopentenone prostaglandins in rat carrageenin pleurisy
Author(s) -
Ianaro Angela,
Ialenti Armando,
Maffia Pasquale,
Pisano Barbara,
Di Rosa Massimo
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)03035-6
Subject(s) - cyclopentenone , pleurisy , inflammation , prostaglandin , prostaglandin e , chemistry , prostaglandin e2 , cyclooxygenase , medicine , lipoxygenase , endocrinology , eicosanoid , pharmacology , biochemistry , enzyme , pleural effusion , organic chemistry , arachidonic acid
In this study, using rat carrageenin‐induced pleurisy, we found that treatment of rats with either indomethacin or NS‐398 suppressed the pleurisy at 2 h but significantly exacerbated this reaction at 48 h. Exacerbated inflammation was associated with reduced prostaglandin D 2 levels, decreased heat shock factor 1 (HSF1) activation, reduced hsp72 expression and increased activation of nuclear factor κB (NF‐κB). Replacement of cyclopentenone prostaglandins by treating rats with either prostaglandin J 2 or prostaglandin D 2 reversed the exacerbating effects of cyclooxygenase inhibitors leading to the resolution of the reaction. In conclusion, we demonstrate that cyclopentenone prostaglandins may act as anti‐inflammatory mediators by inducing in inflammatory cells HSF1‐dependent hsp72 expression and NF‐κB inhibition, two crucial events for the remission of inflammation.

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