ArticleLipids in health and disease2025
Nitroxoline mitigates hepatic steatosis by enhancing cholesterol efflux and promoting bile acid synthesis through LRH-1 signaling.
Article in Lipids in health and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Neohesperidin Regulates Lipid Metabolism and Ameliorates MASLD by Targeting ECHS1.Phytotherapy research : PTR · 2026Article
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Abstract
backgroundMetabolic associated fatty liver disease (MAFLD) has emerged as the most common chronic liver disease worldwide. However, effective pharmacological treatments remain limited. Dysregulated lipid metabolism and impaired bile acid synthesis are recognized as key contributors to the pathogenesis of MAFLD. This study aimed to investigate the therapeutic potential and underlying mechanisms of nitroxoline (Nit), an antimicrobial agent identified through drug repurposing, in ameliorating hepatic steatosis.
methodsNit was administered to high-fat diet (HFD)-fed low-density lipoprotein receptor knockout (Ldlr
resultsNit treatment significantly reduced liver weight without affecting body weight in HFD-fed Ldlr⁻/⁻ mice. Serum total cholesterol, low-density lipoprotein (LDL)-cholesterol, and triglyceride levels were markedly decreased. Mechanistically, Nit enhanced the expression of ATP-binding cassette subfamily G5 (ABCG5) and G8 (ABCG8) transporters, along with cholesterol 7α-hydroxylase (CYP7A1), thereby promoting cholesterol efflux into bile and bile acid synthesis. In Huh-7 cells, Nit induced ABCG5, ABCG8 and CYP7A1 expression in a dose-dependent manner. Furthermore, RNA-Seq analysis revealed liver receptor homolog-1 (LRH-1) as a potential transcriptional regulator related to Nit. Notably, pretreatment with the LRH-1 inhibitor, ML-180 abolished Nit-induced upregulation of ABCG5, ABCG8 and CYP7A1, suggesting that Nit may alleviate hepatic lipid accumulation primarily through LRH-1 activation.
conclusionsThis study identifies Nit as a promising pharmacological candidate for MAFLD by modulating cholesterol metabolism and bile acid synthesis through LRH-1-mediated activation. These findings not only advance the understanding of metabolic liver disease pathogenesis but also support the development of innovative and accessible therapeutic strategies by leveraging existing compounds to improve health outcomes.
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