Effects of lipopolysaccharides on placental oxidative stress and angiogenic factors: fetal repercussion

Abstract

Disturbances during intrauterine development are linked to fetal growth retardation and programming of diseases at adult life. Placental oxidative stress and placental impaired angiogenesis may be underlying mechanisms. It was investigated whether maternal inflammation, induced by lipopolysaccharides (LPS) elevates oxidative stress and affects vascular endothelial growth factor (VEGF) in placenta of rats. LPS was administered in pregnant Wistar rats at days 13, 15, 17 and 19 of pregnancy, accompanied or not by α‐tocopherol treatment during all pregnancy. At 20th day of gestation, fetal and placental weights were not affected by LPS, however placental and fetal hepatic lipid peroxidation was increased, as well as, placental and maternal hepatic reduced glutathione (GSH) levels were lowered. Moreover, LPS treatment increased VEGF and VEGF receptor type‐1 (VEGFR‐1) expression. Maternal α‐tocopherol treatment prevented lipid peroxidation changes induced by LPS, albeit it did not recover GSH levels or changed expressions of VEGF and VEGFR‐1. Thus, although LPS increases oxidative stress, it may increase placental angiogenesis. CAPES, CNPq and FACEPE.