Neuroprotective Potential of Thyme Essential Oil against Beta-Amyloid Toxicity in SH-SY5Y Cells

Abstract

Alzheimer disease (AD) is a chronic neurodegenerative disorder characterized by progressive neuronal loss, with beta-amyloid (Aβ) accumulation playing a pivotal role in its pathology. Recent attention has turned toward naturally derived agents for their potential in mitigating neurotoxicity associated with AD. Thyme essential oil (EO), rich in bioactive compounds such as thymol and carvacrol, has demonstrated therapeutic effects in various inflammatory and oxidative disease models, but its direct neuroprotective potential against Aβ-induced toxicity remains underexplored. In this study, we investigated the effect of thyme EO on Aβ25–35-induced cytotoxicity in SH-SY5Y human neuroblastoma cells. The cells were exposed to Aβ with or without prior treatment using thyme EO (50–200 μg/mL). Cell viability was determined by 3-(4,5-dimetyhylthiazol-2-yl)-2,5-diphenylterazolium bromide assay, and molecular assessments of apoptosis and oxidative stress were performed using terminal deoxynucleotidyl transferase dUTP nick end labeling staining, dichlorofluorescein diacetate assay, and western blot analysis. Pretreatment with thyme EO significantly improved cell viability, reduced Aβ-induced apoptosis markers, including cleaved caspase-3 and altered ratio of Bcl-2-associated X protein (Bax) to B-cell lymphoma 2 (Bcl-2), and diminished DNA fragmentation. Additionally, thyme EO attenuated intracellular reactive oxygen species levels. Mechanistically, thyme EO promoted the phosphorylation of nuclear factor erythroid 2-related factor 2, leading to increased expression of antioxidant enzymes, including heme oxygenase-1 and superoxide dismutase. These data suggest that thyme EO alleviates Aβ-induced neuronal stress by modulating redox signaling and apoptotic pathways. Thus, thyme EO may serve as a promising candidate for therapeutic development targeting oxidative and apoptotic mechanisms in AD.