Saturated and unsaturated fatty acids differentially regulate in vitro and ex vivo placental antioxidant capacity

摘要

Problem Complications from prematurity are the leading cause of death among children under 5?years of age. Although clinical studies have shown a positive correlation between maternal high‐fat diet (HFD) and preterm birth (PTB), the underlying mechanisms remain to be elucidated. Furthermore, it remains unclear how fatty acid type influences the effects of bacterial endotoxins. Method of study HTR‐8/SVneo trophoblasts were cultured in either 0.5?mmol?L ?1 palmitic acid (PA) or linoleic acid (LA) in the absence or presence of 100?μg?mL ?1 of lipopolysaccharide (LPS) or lipoteichoic acid (LTA). Murine placental explants were cultured in either 2?mmol?L ?1 PA or LA, and cell viability, total antioxidant capacity (TAC), lipid peroxidation, H 2 O 2 , heme oxygenase‐1 (HO‐1), and nuclear erythroid 2‐related factor 2 (Nrf‐2) and nuclear factor‐kappa light‐chain enhancer of activated B cells (NF‐κB) transcription factor activity assays were assessed. Results Palmitic acid significantly (i) increased cell death, (ii) decreased TAC, and (iii) increased lipid peroxidation; but did not significantly increase HO‐1. In contrast, LA maintained cell viability and significantly increased TAC and HO‐1 . In addition, incubating placental explants with PA significantly increased NF‐κB activity. Co‐incubating cells with PA and LPS or LTA significantly potentiated H 2 O 2 production and increased lipid peroxidation . Co‐incubating cells with PA and LTA synergistically impaired TAC, and LTA decreased TAC more so than LPS. Co‐incubation with PA/LA and LPS/LTA decreased HO‐1 levels compared to treatment with either fatty acid alone. Conclusion Our findings suggest that saturated and unsaturated fats differentially regulate placental viability, antioxidant capacity, and inflammation and the actions of gram‐positive and gram‐negative endotoxins.