ArticleEnvironmental science and pollution research international2022
Role of Platelet-activating factor and HO-1 in mediating the protective effect of rupatadine against 5-fluorouracil-induced hepatotoxicity in rats.
Article in Environmental science and pollution research international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 15 citations in OpenAlex.
- Rupatadine Ameliorates Cisplatin-Induced Hepatotoxicity in Rats: Targeting HMGB1/TLR4/NF-κB and NLRP3/Caspase-1 Signaling Pathways.Journal of biochemical and molecular toxicology · 2026Article
- Repurposing rupatadine to attenuate ovarian ischemia reperfusion in rats through modulation of PAF/NF-κB/TNF-α/IL-1β; HIF-1α/VEGF/Caspase 3 signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Modulating platelet-activating factor by rupatadine attenuates gentamicin-induced nephrotoxicity in rats via NF-κB/caspase-3 and Nrf2/HO-1 signaling cascades.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Thymol Protects against 5-Fluorouracil-Induced Hepatotoxicity via the Regulation of the Akt/GSK-3β Pathway in In Vivo and In Silico Experimental Models.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Hepatoprotective effect of Nobiletin against 5-fluorouracil induce hepatotoxicity.Current research in pharmacology and drug discovery · 2024Article
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6 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
5-fluorouracil (5-FU) is a widely used chemotherapeutic drug, but its hepatotoxicity challenges its clinical use. Thus, searching for a hepatoprotective agent is highly required to prevent the accompanied hepatic hazards. The current study aimed to investigate the potential benefit and mechanisms of action of rupatadine (RU), a Platelet-activating factor (PAF) antagonist, in the prevention of 5-FU-related hepatotoxicity in rats. Hepatotoxicity was developed in male albino rats by a single 5-FU (150 mg/kg) intra-peritoneal injection on the 7th day of the experiment. RU (3 mg/kg/day) was orally administrated to the rodents for 10 days. Hepatic toxicity was assessed by measuring both liver and body weights, serum alanine aminotransferase and aspartate aminotransferase (ALT and AST), hepatic oxidative stress parameters (malondialdehyde (MDA), nitric oxide levels (NOx), reduced glutathione (GSH), superoxide dismutase (SOD)), and heme oxygenase-1 (HO-1). Inflammatory markers expressions (inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNFα), interleukins; IL-1B, IL-6), the apoptotic marker (caspase-3), and PAF were measured in the hepatic tissue. 5-FU-induced hepatotoxicity was proved by the biochemical along with histopathological assessments. RU ameliorated 5-FU-induced liver damage as proved by the improved serum ALT, AST, and hepatic oxidative stress parameters, the attenuated expression of hepatic pro-inflammatory cytokines and PAF, and the up-regulation of HO-1. Therefore, it can be concluded that RU pretreatment exerted a hepatoprotective effect against 5-FU-induced liver damage through both its powerful anti-inflammatory, antioxidant, and anti-apoptotic effect.
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