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    Acyclovir provides protection against 6-OHDA-induced neurotoxicity in SH-SY5Y cells through the kynurenine pathway
    (Elsevier, 2025) Sezen, Selma; Karadayi, Mehmet; Yesilyurt, Fatma; Burul, Feyza; Gulsahin, Yusuf; Ozkaraca, Mustafa; Okkay, Ufuk
    Parkinson's disease is one of the most prevalent neurodegenerative disorders worldwide. The kynurenine pathway associated with oxidative stress and neuroinflammation is recognized to contribute to its pathophysiology, although the exact mechanism is not fully elucidated. In neuroinflammation, IDO-1 catalyzes the conversion of tryptophan to neurotoxic QUIN through the kynurenine pathway. Consequently, QUIN increases oxidative stress via nNOS and NMDA, which causes neurodegeneration. Few studies have reported on the effect of different antiviral drugs in Parkinson's disease; the exact mechanism is still unknown. The antiviral acyclovir has been shown to have neuroprotective properties and can cross the blood-brain barrier. We examined acyclovir's effects and potential mechanisms in the 6-OHDA-induced in vitro model of Parkinson's disease in SHSY5Y cells using biochemical, immunocytochemical, and in silico methods. MTT assay demonstrated that acyclovir significantly decreased cell mortality induced by the neurotoxic 6-OHDA at dosages of 3.2 mu M, 6.4 mu M, 12.8 mu M, 25.6 mu M, and 51.2 mu M. In immunocytochemical analysis, acyclovir treatment decreased alpha-synuclein and TNF-alpha expressions in cells. In biochemical analyses, while IL-17A and TOS levels decreased depending on varying doses (1.6 mu M, 3.2 mu M, 6.4 mu M, 12.8 mu M), TAC levels increased. Using in silico analyses to investigate the mechanism showed that acyclovir docked with TNF-alpha, IL-17A, IDO-1, nNOS, alpha-synuclein, and NMDA. The findings demonstrated that acyclovir had neuroprotective effects by modulating the kynurenine pathway and decreasing neurodegeneration via QUIN inhibition in an in vitro Parkinson's disease model. Although the