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Purpose: To investigate the role of nicotinamide phosphoribosyltransferase (NAMPT) in lipopolysaccharide (LPS)-induced damage in trophoblastic HTR-8/SVneo cells (HTR8 cells), with the aim of ultimately providing new therapeutic targets of preeclampsia (PE).
Methods: Trophoblastic HTR-8/SVneo was cultured and treated with LPS to mimic PE in vitro, while FK866, an antagonist of NAMPT, was used to establish an inflammatory model of HTR8 cells. Western blot, enzyme-linked immunosorbent assay (ELISA) and quantitative real-time-polymerase chain reaction (qRT-PCR) were used to evaluate inflammatory response in HTR8 cells, and cell counting kit-8 (CCK8) and oxidative stress kits were performed to quantify cell activity in HTR cells.
Results: Compared with the control group, the administration of LPS significantly increased the expression levels of NAMPT in HTR8 cells. FK866 suppressed the expression levels of proinflammatory factors IL-1β, TNF-α and IL-6, and alleviated inflammation by inhibiting NAMPT-mediated NF-κB pathway. The antioxidant effect of FK866 was achieved via activation of antioxidant proteins,
catalase (CAT) and glutathione (GSH).
Conclusion: FK866 protects HTR8 cells from LPS-induced inflammation and oxidative stress through the inhibition of NAMPT-NF-κB signaling pathway. Thus, NAMPT is a potential therapeutic target for preeclampsia (PE).