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For 18\u00a0days, Lura (1 and 3\u00a0mg\/kg) was given orally, starting 7\u00a0days before giving six doses of Dox (2.5 mg\/kg every other day, i.p).\u00a0Lura attenuated Dox-instigated cardiac injury as assured by the decrease in cardiac troponin-I (cTn-I), kg) and creatine kinase MB (CK-MB) levels. In addition, Lura remarkably declined Dox-triggered neuronal dysfunction, as confirmed by diminished anxiety and depression-alike behaviors in the open field (OFT) and forced swimming (FST) tests, respectively. Furthermore, Lura replenished cardiac and brain antioxidant markers, mitochondrial modulator, PGC-1\u03b1, and significantly decreased inflammatory mediators, miR34a-5p, and pro-apoptotic caspase-3 levels. In the brain, Lura also mitigated the induction of glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor-1 (Iba-1). In the same context, Lura pretreatment upregulated the brain-derived neurotrophic factor (BDNF)\/tropomyosin receptor kinase B (TrkB)\/phosphoinositide 3-kinase (PI\n                    <jats:sub>3<\/jats:sub>\n                    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.\n                  <\/jats:p>","DOI":"10.1007\/s00210-026-05019-z","type":"journal-article","created":{"date-parts":[[2026,3,31]],"date-time":"2026-03-31T02:43:19Z","timestamp":1774924999000},"page":"13731-13757","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Repurposing lurasidone to alleviate doxorubicin-induced cardiotoxicity and neurotoxicity via BDNF\/TrkB\/PI3K\/Akt\/CREB and miR-34a-5p\/PGC-1\u03b1 pathways"],"prefix":"10.1007","volume":"399","author":[{"given":"Nermeen A.","family":"Bayoumy","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abeer","family":"Elkhoely","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shimaa K.","family":"Mohamed","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,3,31]]},"reference":[{"issue":"2021","key":"5019_CR1","doi-asserted-by":"publisher","first-page":"1635","DOI":"10.3390\/pharmaceutics13101635","volume":"13","author":"H Abbas","year":"2021","unstructured":"Abbas H, Gad A, Khattab MA, Mansour M (2021) The tragedy of Alzheimer\u2019s disease: towards better management via resveratrol-loaded oral bilosomes. 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