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Strathprints serves world leading Open Access research by the University of Strathclyde, including research by the Strathclyde Institute of Pharmacy and Biomedical Sciences (SIPBS), where research centres such as the Industrial Biotechnology Innovation Centre (IBioIC), the Cancer Research UK Formulation Unit, SeaBioTech and the Centre for Biophotonics are based.

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7β-hydroxy-epiandrosterone modulation of 15-deoxy-Δ12,14-prostaglandin J2, prostaglandin D2 and prostaglandin E2 production from human mononuclear cells

Davidson, Jillian and Wulfert, Ernst and Rotondo, Dino (2008) 7β-hydroxy-epiandrosterone modulation of 15-deoxy-Δ12,14-prostaglandin J2, prostaglandin D2 and prostaglandin E2 production from human mononuclear cells. Journal of Steroid Biochemistry and Molecular Biology, 112 (4-5). pp. 220-227. ISSN 0960-0760

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Abstract

7β-hydroxy-epiandrosterone (7β-OH-EPIA) has been shown to be cytoprotective in various organs including the brain. It has also been shown that prostaglandin D2 (PGD2) and its spontaneous metabolite 15-deoxy--12,14-prostaglandin J2 (15d-PGJ2) are also cytoprotective. It is possible that these prostaglandins derived from circulating mononuclear cells may mediate the actions of 7β-OH-EPIA. The aim of this study, therefore, was to ascertain the effect of 7β-OH-EPIA (in the absence or presence of tumour necrosis factor-α (TNF-α)), a pro-inflammatory stimulus, on the biosynthesis of PGD2, PGE2 and 15d-PGJ2 from human mononuclear cells. Prostaglandins were measured by enzyme immunoassay (EIA). 7β-OH-EPIA alone induced a concentration-dependant increase in the production of PGD2. TNF-α increased PGD2 levels which were enhanced by 7β-OH-EPIA. 7β-OH-EPIA increased 15d-PGJ2 levels both in the absence and presence of TNF-α. 7β-OH-EPIA alone had no effect on PGE2 biosynthesis but suppressed TNF-α-induced PGE2 circa 50%. 7β-OH-EPIA also increased the level of free arachidonic acid and radiolabelled prostaglandins in cells pre-incubated with radiolabelled arachidonic acid, indicating that the increase may occur via the enhanced release of substrate arachidonic acid. 7β-OH-EPIA did not affect levels of the anti-inflammatory cytokine IL-10 indicating that this is an unlikely mechanism by which 7β-OH-EPIA induces its actions but more likely exerts its effects via the production of cytoprotective prostaglandins.