ArticleMolecular biology reports2026
Ebastine mitigates cisplatin-induced pulmonary injury associated with alterations in the miR-101/PI3K/mTOR/ULK1 signaling 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
backgroundEbastine (EBT), a second-generation antihistamine, exhibits notable antioxidant and anti-inflammatory effects. EBT may serve as a promising therapeutic candidate for limiting drug-induced lung injury. This study investigated the protective effects of EBT against cisplatin-associated pulmonary toxicity and explored the underlying mechanisms of this protection. The disturbance of autophagy via the dysregulated PI3K/mTOR/ULK1 pathway was evaluated as well as its influence on pulmonary toxicity.
methodsThis study examined the effects of EBT (1 mg/kg orally) on pulmonary injury induced by cisplatin (7.5 mg/kg I.P.) in rats. Pulmonary tissue levels of oxidative stress and inflammatory markers were measured, while histopathological alterations and collagen deposition were examined using hematoxylin and eosin staining and Masson's trichrome staining, respectively. The molecular mechanisms by which EBT mitigates pulmonary injury were investigated.
resultsThe findings demonstrated that EBT ameliorated pulmonary function by suppressing the observed pathological tissue changes. EBT exhibited antioxidant and anti-inflammatory properties through decreasing levels of several evaluated proinflammatory markers while enhancing levels of anti-inflammatory enzymes and interleukins. Furthermore, EBT treatment was associated with reduced expression of AMPK, TSC1, TSC2, PI3K, PDK1, CD36, and IGF-1, and with increased expression of miRNA-101 and ULK1, as demonstrated by Western blotting and PCR. Additionally, the effect on pulmonary tissue viability was underscored by elevated Bcl-2 levels and reduced caspase-3 staining in immunohistopathological analysis.
conclusionsEBT effectively attenuated cisplatin-induced pulmonary injury in rats, and these protective effects were associated with modulation of oxidative stress, inflammatory responses, and alterations in the miR-101/PI3K/mTOR/ULK1 signaling axis. Further mechanistic and clinical investigations are warranted to confirm these molecular interactions and evaluate therapeutic applicability in patients.
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