Repurposing lurasidone to alleviate doxorubicin-induced cardiotoxicity and neurotoxicity via BDNF/TrkB/PI3K/Akt/CREB and miR-34a-5p/PGC-1α pathways

K) alleyway, along with the downstream proteins, the phosphorylated form of kinase B (p-Akt), and phosphorylated cAMP-response element binding form (p-CREB). The previously mentioned results were confirmed by histological examination and toluidine blue staining. Taken together, Lura conferred its cardioprotective and neuroprotective effects on Dox-treated rats through the enhancement of the BDNF/TrkB/PI3K/Akt/CREB signaling pathway, along with downregulation of miR 34a-5p leading to alleviated oxidative stress, inflammation, mitochondrial dysfunction, and apoptosis.