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Thymol protects against 6-hydroxydopamine-induced neurotoxicity in in vivo and in vitro model of Parkinson’s disease via inhibiting oxidative stress

BACKGROUND: Parkinson’s disease (PD) is a multifactorial movement disorder with the progressive degeneration of the nigrostriatal system that impairs patients’ movement ability. Oxidative stress has been found to affect the etiology and pathogenesis of PD. Thymol, a monoterpenic phenol, is one of th...

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Detalles Bibliográficos
Autores principales: Nourmohammadi, Saeideh, Yousefi, Sanaz, Manouchehrabadi, Mahboubeh, Farhadi, Mona, Azizi, Zahra, Torkaman-Boutorabi, Anahita
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8832724/
https://www.ncbi.nlm.nih.gov/pubmed/35144603
http://dx.doi.org/10.1186/s12906-022-03524-1
Descripción
Sumario:BACKGROUND: Parkinson’s disease (PD) is a multifactorial movement disorder with the progressive degeneration of the nigrostriatal system that impairs patients’ movement ability. Oxidative stress has been found to affect the etiology and pathogenesis of PD. Thymol, a monoterpenic phenol, is one of the most important dietary constituents in thyme species. It has been used in traditional medicine and possesses some properties including antioxidant, free radical scavenging, anti-inflammatory. In this study, in vitro and in vivo experiments were performed with the thymol in order to investigate its potential neuroprotective effects in models of PD. METHODS: The present study aimed to evaluate the therapeutic potential of thymol in 6-hydroxydopamine (6-OHDA)-induced cellular and animal models of PD.  RESULTS: Post-treatment with thymol in vitro was found to protect PC12 cells from toxicity induced by 6-OHDA administration in a dose-dependent manner by (1) increasing cell viability and (2) reduction in intracellular reactive oxygen species, intracellular lipid peroxidation, and annexin-positive cells. In vivo, post-treatment with thymol was protective against neurodegenerative phenotypes associated with systemic administration of 6-OHDA. Results indicated that thymol improved the locomotor activity, catalepsy, akinesia, bradykinesia, and motor coordination and reduced the apomorphine-caused rotation in 6-OHDA-stimulated rats. Increased level of reduced glutathione content and a decreased level of MDA (malondialdehyde) in striatum were observed in the 6-OHDA rats post-treated with thymol. CONCLUSIONS: Collectively, our findings suggest that thymol exerts protective effects, possibly related to an anti-oxidation mechanism, in these in vitro and in vivo models of Parkinson’s disease.