ArticleMolecular biology reports2026
Methylene blue confers protection against hepatotoxicity induced by Cisplatin; the involvement of oxidative stress, apoptosis and NCOA4-mediated ferritinophagy.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCisplatin (Cisp) is a common chemotherapeutic drug that has demonstrated effectiveness against number of cancers. However, its dose-limiting toxicities, such as hepatotoxicity, limit its therapeutic usefulness. Methylene blue (MB), a substance derived from phenothiazine, has significant antioxidant qualities. This study investigated the protective effects of Methylene blue (MB) against Cisplatin-induced hepatotoxicity and the involvement of the anti-inflammatory, the anti-oxidant and the iron regulating effects in male Wistar.
methodsAlbino rats. Rats were divided into four groups: control, Cisplatin (Cisp, 8 mg/kg, IP), and two MB-treated groups (25 mg/kg and 50 mg/kg, IP) with Cisp.
resultsCisp administration (8 mg/kg, IP) significantly impaired liver function, increased oxidative stress, promoted apoptosis (increased BAX, CASPASE-3, and decreased BCL2) and disrupted homeostasis by increasing the ferroptosis upstream ferritinophagy (decreased ferritin and increased NCOA4). Treatment with MB at doses of 25 mg/kg and 50 mg/kg demonstrated dose-dependent hepatoprotective effects. The higher dose (50 mg/kg) of MB effectively restored liver function markers, antioxidant status, hindered apoptosis and regulated iron regulatory proteins (ferritin and NCOA4 that reflects ferritinophagy) to levels comparable with the control group. MB treatment significantly reduced lipid peroxidation inhibited apoptotic pathways, and modulated iron-related gene expression. The 50 mg/kg dose consistently outperformed the 25 mg/kg dose across all measured parameters.
conclusionThese findings suggest that MB, particularly at higher doses, may serve as a promising therapeutic agent in mitigating Cisp-induced hepatotoxicity by reducing oxidative stress, regulating iron homeostasis/ferritinophagy/ferroptosis, and inhibiting apoptotic pathways.
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