Placental oxidative stress and inflammation play key roles in the pathophysiology of placental-related disorders. Protection from oxidative stress is provided by antioxidant enzymes which inactivate reactive oxygen species. Omega-3 (n3) polyunsaturated fatty acids (PUFAs) are proposed to have both anti-inflammatory and antioxidant properties. Here, we tested the hypothesis that dietary n3-PUFA intake reduces the oxidative and inflammatory status of the placenta.
Pregnant rats consumed a high n3-PUFA (Hn3) or control diet from day 1 of pregnancy. Fetuses and placentas were collected on days 17 and 22 (term = day 23), and placentas were dissected into junctional (JZ) and labyrinth (LZ) zones. Placental oxidative status was measured by F2-isoprostane concentration, and placental gene expression of antioxidant enzymes Cat, Sod2, Txn1, Pxn1, Pxn5 and Gpx3, and of pro-inflammatory mediators Tnfα, IL-6, IL-1β, Cox1 and Cox2 were measured by qRT-PCR (males only).
Hn3 consumption increased fetal (P<0.05) and placental (P=0.05) weights at day 22 (6.2% and 10.6%, respectively). The Hn3 diet decreased the concentration of F2-isoprostanes in LZ on days 17 (28%; P<0.001) and 22 (8%, P<0.05), and in JZ at day 22 (25%; P<0.05). Hn3 intake increased placental expression of Cat in LZ at both days (P<0.001), but decreased Pxn5 in LZ (P<0.05) at day 17, and decreased Cat, Sod2 and Pxn1 in JZ at day 17 (P<0.05, P<0.001 and P<0.05, respectively). Surprisingly, LZ expression of IL-6 (2.7-fold, P<0.05) and IL-1β (1.7-fold, P<0.05) were both increased by Hn3 diet at day 22.
Dietary n3-PUFA supplementation increased fetal and placental growth, and this effect was associated with reduced placental oxidative status. The Hn3 diet clearly enhanced LZ expression of Cat, whereas it reduced JZ expression of Cat and other antioxidant enzymes. Pro-inflammatory cytokine gene expression was increased by the Hn3 diet at day 22, possibly linked to approaching parturition.