Effects of serum from patients with early-onset pre-eclampsia, HELLP syndrome, and antiphospholipid syndrome on fatty acid oxidation in trophoblast cells.
Słowa kluczowe
Abstrakcyjny
OBJECTIVE
The role of metabolic disorders of long-chain fatty acid oxidation in the development of pre-eclampsia (PE), hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome and antiphospholipid syndrome (APS) is unclear. The aim of this study was to research the effects of three serum on fatty acid oxidation in trophoblast cells.
METHODS
Primary human trophoblast cells and HTR8/SVneo cells were treated with serum from patients with early-onset severe PE (E-PE), E-PE with HELLP (PE-HELLP), APS, and normal pregnant women as controls (NC). Cells treated with free fatty acids (FFAs) of various lengths were used as controls.
RESULTS
Triglyceride (TG) and FFA levels of the E-PE and APS groups were significantly higher than the PE-HELLP and NC groups (P < 0.05). Trophoblast cells treated with serum from the E-PE and APS groups showed obvious morphological changes and a large amount of lipid droplet deposition. Cells in the E-PE group had more severe damage of mitochondria ultrastructure, presenting with cell morphological changes, lipid droplet deposition, and mitochondria damage similar to the long-chain FFA group. FFA levels in the PE-HELLP group increased significantly compared with the NC group (P < 0.05), while TG levels did not change significantly (P > 0.05). Trophoblast cells treated with serum from the PE-HELLP group showed cellular morphology and mitochondria changes similar to the E-PE group, but had relatively less lipid droplet deposition.
CONCLUSIONS
Serum from patients with E-PE, PE-HELLP, and APS with elevated levels of FFA had different effects on trophoblast cells, including cell morphology, lipid droplets deposition, and mitochondrial ultrastructure, suggesting disorders of lipid metabolism and fatty acid oxidation of various degrees and types. Serum from patients with E-PE led to damage similar to that of long-chain FFA in cell morphology, lipid droplet deposition and mitochondrial ultrastructure, indicating the correlation between disorders of long-chain fatty acid oxidation and the development of the disease.
