Correlation of long-chain fatty acid oxidation with oxidative stress and inflammation in pre-eclampsia-like mouse models

•Preeclampsia has been further recognized as a syndrome during pregnancy.•Long-chain fatty acid oxidation (FAO) disorders may be associated with some of preeclampsia.•We investigated the role of FAO and its relationship with oxidative.•FAO disorders were involved in the pathogenesis of pre-eclampsia.

IntroductionPre-eclampsia has been further recognized as a syndrome during pregnancy. Recent studies have found that long-chain fatty acid oxidation (FAO) disorders may be associated with some of pre-eclampsia. However, the mechanism remains unclear. In this study, we investigated the role of FAO and its relationship with oxidative stress and inflammatory signaling pathways in the pathogenesis of pre-eclampsia.MethodsPE-like groups included ApoC3 transgenic mice with abnormal fatty acid metabolism, classical PE-like models with injection of Nω-nitro-l-arginine-methyl ester (L-NA) or lipopolysaccharide (LPS), and antiphospholipid syndrome (APS) mouse model with β2GPI injection. The control group included wild-type mice with normal saline injection. Serum FFA was compared and placental and hepatic LCHAD, p47phox and NF-κB mRNA and protein were detected using real-time quantitative PCR and western blot.ResultsFFA levels were significantly increased and were positively correlated with P47phox and NF-κB mRNA and protein expression in liver of all groups (p < 0.05), except LPS group (p < 0.05) as compared to control. LCHAD mRNA and protein expression in the liver and placenta was significantly increased in ApoC3+NS, ApoC3+L-NA, and β2GPI group, whereas decreased in L-NA group (p < 0.05) as compared to the control group. P47phox mRNA, NF-κB mRNA, and protein expression in the liver of all groups, except in LPS and in the placenta of β2GPI and L-NA groups, significantly increased (p < 0.05). Discussion: FAO disorders were involved in the pathogenesis of pre-eclampsia through oxidative stress and inflammatory endothelial cell injury.