Z Cheng1, M Elmes, S Kirkup, D R E Abayasekara, D C Wathes. 1. Department of Veterinary Basic Sciences, Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield, Herts.,UK. zcheng@rvc.ac.uk
Abstract
OBJECTIVE: To use an in vitro model of the ovine placenta to determine effects of n-6 polyunsaturated fatty acid (PUFA) supplementation on prostaglandin (PG) production. PGs are key regulators of fetal maturation and parturition. STUDY DESIGN: Fetal allantochorion tissue (FC) was collected in late pregnancy (day 135). FC cells were isolated and cultured with 0-100 μM of linoleic acid (LA), γ-linolenic acid (GLA) or arachidonic acid (AA) in serum free medium and challenged with control medium, lipopolysaccharide (LPS, 0.1 μg/ml), dexamethasone (DEX, 5 μM) or a combination of LPS (0.1 μg/ml) with DEX (5 μM). Spent medium was harvested at 2 h and 24 h post challenge for measuring PGs. MAIN OUTCOME MEASURES: To assess the effects of treatment on placental 1- and 2-series PGE production. RESULTS: LA supplementation inhibited both PGE(1) and PGE(2) production. GLA predominantly stimulated PGE(1) generation, although it also increased PGE(2) production. AA supplementation predominantly increased PGE(2) production, but also stimulated PGE(1). DEX treatment with or without LPS inhibited PG production. Supplementation with n-6 PUFAs attenuated or neutralised the stimulatory effect of LPS challenge on FC cells for both PGE(1) and PGE(2) production. CONCLUSION: These data show that supplementation with n-6 PUFAs alters placental PG production, but their precise effects depend on their position in the biosynthetic pathway for PG synthesis. This study supports the possibility that GLA containing oils, widely promoted as dietary supplements, might reduce the risk of pre-term labour by inhibiting the responsiveness of PGE(2) production to LPS challenge in the placenta.
OBJECTIVE: To use an in vitro model of the ovine placenta to determine effects of n-6 polyunsaturated fatty acid (PUFA) supplementation on prostaglandin (PG) production. PGs are key regulators of fetal maturation and parturition. STUDY DESIGN: Fetal allantochorion tissue (FC) was collected in late pregnancy (day 135). FC cells were isolated and cultured with 0-100 μM of linoleic acid (LA), γ-linolenic acid (GLA) or arachidonic acid (AA) in serum free medium and challenged with control medium, lipopolysaccharide (LPS, 0.1 μg/ml), dexamethasone (DEX, 5 μM) or a combination of LPS (0.1 μg/ml) with DEX (5 μM). Spent medium was harvested at 2 h and 24 h post challenge for measuring PGs. MAIN OUTCOME MEASURES: To assess the effects of treatment on placental 1- and 2-series PGE production. RESULTS: LA supplementation inhibited both PGE(1) and PGE(2) production. GLA predominantly stimulated PGE(1) generation, although it also increased PGE(2) production. AA supplementation predominantly increased PGE(2) production, but also stimulated PGE(1). DEX treatment with or without LPS inhibited PG production. Supplementation with n-6 PUFAs attenuated or neutralised the stimulatory effect of LPS challenge on FC cells for both PGE(1) and PGE(2) production. CONCLUSION: These data show that supplementation with n-6 PUFAs alters placental PG production, but their precise effects depend on their position in the biosynthetic pathway for PG synthesis. This study supports the possibility that GLA containing oils, widely promoted as dietary supplements, might reduce the risk of pre-term labour by inhibiting the responsiveness of PGE(2) production to LPS challenge in the placenta.