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Original Research Article | OPEN ACCESS

Nicotinamide phosphoribosyltransferase inhibitor is a potential therapeutic target in LPS-induced human trophoblast cell injury

Zuoman Zhang, Lijun Tang, Meifang Huang, Guangliang Bi, Weimin Huang

Department of Neonatology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China;

For correspondence:-    

Accepted: 28 July 2023        Published: 31 August 2023

Citation: Zhang Z, Tang L, Huang M, Bi G, Huang W. Nicotinamide phosphoribosyltransferase inhibitor is a potential therapeutic target in LPS-induced human trophoblast cell injury. Trop J Pharm Res 2023; 22(8):1579-1585 doi: 10.4314/tjpr.v22i8.8

© 2023 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

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 pro-inflammatory 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).

Keywords: HTR8/SVneo cells, Nicotinamide phosphoribosyltransferase, FK866, Inflammation, Pre-eclampsia

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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