Neuroprotective Effects of <i>Rosa damascena</i> Essential Oil Against Ethanol-Induced Toxicity in Neural Progenitor Cells
Loading...
Date
Journal Title
Journal ISSN
Volume Title
Publisher
Brieflands
Abstract
Background: Neural progenitor cells (NPCs) in specific regions of the adult brain hold promise for treating central nervous system (CNS) disorders and degenerative diseases, such as Parkinson's and Alzheimer's. Rosa damascena, enriched with flavonoids, offers restorative, inhibitory, and protective advantages against nerve damage. Objectives: This study investigates the neuroprotective effects of R. damascena essential oil (ESO) on NPCs exposed to ethanol (ETH)-induced toxicity. Methods: The study involved two phases: The NPCs were isolated from the brains of young Wistar rats and cultured following standard protocols. Differentiation into mature neural cells (NCs) was induced by withdrawing supportive factors. MTT assays were used to determine effective ETH and ESO doses, followed by assessments of their impact on NPCs and NCs. Gene expression analysis of neuroepithelial stem cell protein (Nestin), Sex determining region Y-box 2 (Sox2), and Paired Box 6 (Pax6) was conducted using real-time PCR during the NPC phase, while class III β-tubulin (Tuj1) and microtubule associated protein 2 (Map2) were evaluated during the NC stage. TAU protein expression was analyzed via immunocytochemistry (ICC). Results: The ETH exposure significantly reduced cell viability in a dose- and time-dependent manner (24, 48, 72 hours), while treatment with 200 µM ESO significantly improved survival in NPCs and NCs (P < 0.001). Additionally, ESO reduced TAU protein expression in NCs exposed to ETH. The NPCs treated with ETH + ESO showed increased expression of Nestin, Sox2, and Pax6 compared to the ETH-only group (P < 0.01). Similarly, Tuj1 and Map2 expression levels were significantly higher in the ETH + ESO group compared to ETH-treated NCs (P < 0.01). Conclusions: The ESO demonstrates significant neuroprotective properties, mitigating ETH-induced toxicity in NPCs and NCs. These findings highlight its potential as a therapeutic agent for reducing neurodegenerative damage and supporting nervous system function.