ArticleTurkish journal of biology = Turk biyoloji dergisi2026
Profiling arbutin as a potent cholinesterase and GSK-3β inhibitor and evaluating its cytotoxicity in SH-SY5Y cells for Alzheimer's disease therapy.
Article in Turkish journal of biology = Turk biyoloji dergisi, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background/aim: Alzheimer's disease (AD) is a neurodegenerative disorder linked to cognitive decline and memory loss, marked by hyperphosphorylated tau tangles and decreased acetylcholine levels, which are affected by acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) activity. Glycogen synthase kinase-3 beta (GSK-3β) also plays a role in AD through abnormal activation. In this study, the potential of β-arbutin to inhibit cholinesterases and GSK-3β was investigated, utilizing in vitro assays, cytotoxicity analysis, and molecular docking simulations to explore its therapeutic implications. Materials and methods: Ellman's technique was used to test the inhibitory effects of arbutin on cholinesterase enzymes. An ATP-Glo luminescent assay kit was used to evaluate the inhibitory effects and inhibition kinetics of arbutin on GSK-3β. A Cell Titer-Glo 2.0 assay kit was used to assess the cytotoxicity of arbutin in SH-SY5Y cells. Results: β-Arbutin exhibited significant inhibitory effects on AChE, BuChE, and GSK-3β, with IC Conclusion: Our research demonstrates that arbutin is a modulator of cholinesterase and GSK-3β and may be beneficial as a multitarget-directed therapeutic natural compound for AD.
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