ArticleJournal of pharmaceutical analysis2026
Gliquidone alleviates DSS-induced ulcerative colitis in rats by targeting carnitine palmitoyltransferase 1A.
Article in Journal of pharmaceutical analysis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Recent advances in the bioanalysis of acylcarnitines: Methodologies, challenges, and clinical perspectives.Pharmaceutical science advances · 2026Review
- Calcined lotus leaf-derived carbon dots: enhanced hemostasis, anti-inflammatory, immunomodulatory properties for ulcerative colitis management.Journal of nanobiotechnology · 2026Article
- Multidisciplinary cutting-edge technologies accelerating target-based drug discovery.Journal of pharmaceutical analysis · 2026Article
- Article
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Authors and funding
9 authors.
Funding
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Abstract
Ulcerative colitis (UC) is an idiopathic, chronic inflammatory disorder with an increasing incidence worldwide. Due to the complex and unclear therapeutic targets, unmet UC therapeutic drugs still exist. Recently, acylcarnitine metabolism disorder has been linked to intestinal inflammation, but its role in UC remains elusive. According to our preliminary non-targeted metabolomics data, acylcarnitines (ACs) was screened as the disturbed metabolites in the different intestinal inflammation-related diseases. Here we quantified 26 ACs within liquid chromatography-tandem mass spectrometry (LC-MS/MS) in the dextran sulfate sodium (DSS)-induced UC rat model, and found that long-chain acylcarnitines (LCACs) were increased to varying degrees. As the key metabolites of fatty acid β-oxidation (FAO), the upstream metabolites long-chain fatty acids (LCFAs) and the related metabolic enzymes were further characterized, the results showed that the rate-limiting enzyme carnitine palmitoyltransferase 1A (CPT1A)-mediated LCFAs-LCACs metabolic axis was activated sharply. Next
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