ArticleMolecular biology reports2026
Gastrodin mitigates cisplatin-induced cardiotoxicity in Swiss albino mice by restoring redox homeostasis and modulating the p62-Keap1-Nrf2 Axis.
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 (CP) chemotherapy can elicit clinically meaningful cardiac injury, and the additional use of effective cardioprotective agents is a pressing need. This study investigated the protective effects and mechanisms of gastrodin against CP-induced cardiotoxicity, through redox-, inflammatory-, apoptotic-, and Nrf2-axis mechanisms.
methodsAdult male Swiss albino mice received CP (5 mg/kg, i.p., Days 3 and 6) with or without oral gastrodin (50 or 100 mg/kg/day) for 7 days. Outcomes included cardiac histology, serum/tissue injury markers, myocardial ATP, oxidative stress indices, cytokines, and qRT-PCR for apoptosis- and Nrf2-pathway genes.
resultsCP produced marked myocardial injury, increasing the histological injury score (p < 0.001), and elevated serum cTnI (p < 0.001). CP depleted myocardial ATP (p < 0.001) and increased lipid peroxidation, as reflected by elevated MDA (p < 0.001). These changes were accompanied by increased TNF-α and IL-6 (p < 0.001). Gastrodin 100 mg/kg significantly attenuated these alterations, reducing the histological injury score, serum cTnI, restoring ATP, and lowering MDA (p < 0.05-0.001 vs. CP). Gastrodin also reduced TNF-α and IL-6 and shifted gene expression toward cytoprotection.
conclusionGastrodin may have a protective activity against CP cardiotoxicity, primarily by restoring redox balance/energy status, suppressing inflammation and apoptosis, and modulating p62-Keap1-Nrf2 related gene expression.
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