ArticleMolecular biology reports2026
Gramicidin A attenuates oxidative stress, mitochondrial dysfunction, DNA damage, and inflammation in 6-OHDA-induced SH-SY5Y cells.
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
backgroundOxidative stress and mitochondrial dysfunction are major contributors to neurodegenerative diseases, and this study investigated the protective potential of Gramicidin A in a 6-hydroxydopamine (6-OHDA)-induced SH-SY5Y cellular injury model relevant to Parkinson's disease (PD). METHODS AND
resultsFollowing the 3-(4,5-Dimethyl-2-thiazolyl)- 2,5-diphenyl-2H-tetrazolium bromide (MTT) assay to determine the appropriate Gramicidin A concentration, cells were evaluated for oxidative stress parameters, including reactive oxygen species (ROS), total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), malondialdehyde (MDA), reduced glutathione (GSH), and glutathione peroxidase (GPx), as well as mitochondrial membrane potential (MMP), the oxidative DNA damage marker 8-hydroxy-2'-deoxyguanosine (8-OHdG), and inflammatory stress markers including interleukin-6 (IL-6), IL-8, and transforming growth factor-beta (TGF-β). Exposure to 6-OHDA significantly reduced cell viability, increased ROS production, and disrupted oxidative balance (p < 0.0001). In contrast, both pre- and post-treatment with Gramicidin A reduced ROS levels, improved TAS, TOS, and OSI values, decreased MDA levels, increased GSH levels, and modulated GPx activity (p < 0.0001) in SH-SY5Y cells. Gramicidin A treatment also modulated the JC-10 red/green fluorescence ratio, suggesting changes in MMP, decreased 8-OHdG levels, and a significant reduction in 6-OHDA-induced elevations in IL-6, IL-8, and TGF-β levels in SH-SY5Y cells (p < 0.0001).
conclusionsThese findings suggest that Gramicidin A attenuates 6-OHDA-induced cellular injury in SH-SY5Y cells by modulating oxidative stress, mitochondrial membrane potential-related changes, oxidative DNA damage, and inflammatory stress responses.
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