Akademik Veri Yönetim Sistemi
Scientific Reports, cilt.16, sa.1, 2026 (SCI-Expanded, Scopus)
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by oxidative stress, neuroinflammation, and α-synuclein accumulation. Activation of the angiotensin II type 1 (AT1) receptor contributes to these pathogenic mechanisms. This study aimed to evaluate the neuroprotective effects of telmisartan, an AT1 receptor antagonist, in a cellular model of PD. An in vitro PD model was established by exposing SH-SY5Y neuroblastoma cells to 200 µM 6-hydroxydopamine (6-OHDA). Cells were pre-treated with varying concentrations of telmisartan prior to toxin exposure. Cell viability was assessed using MTT and LDH assays. Oxidative stress markers, including malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH), were measured. Inflammatory mediators and apoptotic markers were analyzed, and α-synuclein and IL-1β expression were evaluated by immunofluorescence. Telmisartan pre-treatment significantly improved cell viability. While 6-OHDA increased MDA levels and reduced antioxidant enzyme activities, telmisartan reversed these effects by attenuating oxidative stress. In addition, telmisartan downregulated pro-inflammatory mediators (TNF-α, IL-6, NF-κB, and caspase-3) and increased IL-10 expression. Immunofluorescence analysis showed that telmisartan suppressed 6-OHDA-induced α-synuclein and IL-1β overexpression. These findings indicate that telmisartan protects SH-SY5Y cells against 6-OHDA-induced neurotoxicity and supports AT1 receptor blockade as a promising neuroprotective strategy for Parkinson’s disease.