ArticleMolecular biology reports2026
Neuroprotective effects of gallic acid in an MPP⁺-induced SH-sy5y cell model of parkinson's disease.
Article in Molecular biology reports, 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
backgroundParkinson's Disease (PD) represents the second most prevalent neurodegenerative condition which leads to the progressive destruction of dopaminergic neurons in the substantia nigra through oxidative stress mechanisms. The research evaluated Gallic Acid (GA) as a natural polyphenol with proven antioxidant properties for its ability to protect cells from 1-methyl-4-phenylpyridinium (MPP⁺)-induced neurotoxicity in SH-SY5Y dopaminergic cell models.
methodsThe research used SH-SY5Y cells which received 1 mM MPP⁺ treatment alongside different GA concentrations (25, 50 and 100 µM) for 24 and 48 h. The CCK-8 assay measured cell viability while flow cytometry evaluated apoptosis and SOD and MDA levels determined oxidative status through SOD and Catalase and NO measurements.
resultsThe addition of MPP⁺ resulted in a 32.74% decrease in cell viability at 48 h while simultaneously decreasing SOD and Catalase and NO levels and increasing MDA levels. The addition of 25 µM GA protected cells from damage by increasing their viability to 86.53% at 48 h and decreasing apoptotic cell numbers. Our results revealed that co-treatment with 25-50 µM GA effectively mitigated oxidative damage by preventing the depletion of catalase and NO levels. Furthermore, GA successfully reduced lipid peroxidation; specifically, 25 µM GA decreased MDA levels from 21.18 to 9.64 nM/mg protein at 48 h, thereby restoring the cellular antioxidant defense system against MPP
conclusionsIn conclusion, the present study demonstrates that GA exerts a significant neuroprotective effect in an in vitro PD model by modulating the endogenous antioxidant network and alleviating lipid peroxidation. By effectively reversing the depletion of crucial enzymes and reducing apoptosis, GA shows potential therapeutic efficacy against oxidative stress-associated neurodegeneration. These findings suggest that GA is a promising phytochemical candidate warranting further in vivo evaluation to clarify its long-term bioavailability and translational value.
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