Thymol Protects Against 6-Hydroxydopamine-Induced Neurotoxicity in in Vivo and in Vitro Model of Parkinson’S Disease Via Inhibiting Oxidative Stress Publisher Pubmed



Nourmohammadi S¹ ; Yousefi S¹ ; Manouchehrabadi M² ; Farhadi M¹ ; Azizi Z³ ; Torkamanboutorabi A^{2, 4} Show Affiliations
Source: BMC Complementary Medicine and Therapies Published:2022

Abstract

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. © 2022, The Author(s).