Neuroprotective Effects of Gallic Acid in an MPP⁺-Induced SH-SY5Y Cell Model of Parkinson’s Disease

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Abstract Background Parkinson’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. Methods and Results The research used SH-SY5Y cells which received 1 mM MPP⁺ treatment alongside different GA concentrations (25,50 and 100 µM) for 24 and 48 hours. 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. The addition of MPP⁺ resulted in a 32.74% decrease in cell viability at 48 hours 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 hours and decreasing apoptotic cell numbers. The protective effects of 25–50 µM GA were observed through its ability to stop Catalase and NO decreases and its successful reduction of MDA levels (GA 25 µM decreased MDA from 21.18 to 9.64 nM/mg prot at 48 hours). The research indicates that GA functions as an antioxidant by rebuilding the body's natural defense system against oxidative stress. Conclusions The study demonstrates that GA provides strong protection against peroxidation by maintaining essential antioxidant enzyme activities in MPP⁺-exposed cells. The research demonstrates that GA shows potential as an effective

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