Lipoic acid attenuated hypoxia-induced disruption of mitochondrial respiration in an in vitro human trophoblast model.

Preeclampsia is a pregnancy-specific hypertensive disorder characterized by abnormal placentation, trophoblast dysfunction, and systemic endothelial injury. Mitochondrial dysfunction and impaired energy metabolism have been implicated in its pathogenesis. This in vitro study investigated the effects of a CoCl2-induced hypoxia-mimetic condition on trophoblast mitochondria and evaluated whether lipoic acid (LA) could mitigate the associated impairment. In HTR-8/SVneo cells, CoCl₂ significantly reduced cell viability and the expression of oxidative phosphorylation (OXPHOS)-related genes. In addition, it impaired mitochondrial respiration by suppressing the oxygen consumption rate. LA markedly restored the reduced expression of OXPHOS-associated genes and modestly improved cell viability, and attenuated mitochondrial membrane potential disruption under the 100 μM CoCl₂ conditions. LA also showed partial recovery of trophoblast migration and TIE2 expression under CoCl₂-induced stress. These findings indicate that LA may partially attenuate CoCl₂-induced mitochondrial and functional impairment in trophoblasts in vitro. Further studies are needed to clarify the underlying mechanisms and the relevance of these findings to preeclampsia.