Ginkgolide B Attenuates 6-Hydroxydopamine-Induced Cellular Damage and Modulates Oxidant-Evoked Ca<sup>2+</sup> Signalling in SH-SY5Y Cells.

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Oxidative stress and disruption of intracellular Ca2+ homeostasis contributes to dopaminergic neuronal damage in Parkinson's disease. In this study, the protective effects of Ginkgolide B (GKB) against 6-hydroxydopamine (6-OHDA)-induced SH-SY5Y cell damage were investigated, with particular attention to oxidant-evoked intracellular Ca2+ signalling. Cells were pre-treated with GKB (20 µg/mL) for 2 h, followed by exposure to 6-OHDA (200 µM) for 24 h. CCK-8-derived metabolic activity, oxidative stress, cell death, PARP-1, caspase-3, and intracellular Ca2+ responses were evaluated using biochemical and fluorescence methods. 6-OHDA decreased CCK-8-derived metabolic activity, GSH, and SOD levels, while increasing MDA, intracellular oxidant-sensitive fluorescence, PI-positive cell ratio, and total PARP-1 and caspase-3 levels. GKB pretreatment significantly attenuated these changes and partially improved cellular redox balance. Furthermore, while 6-OHDA enhanced the H2O2-stimulated intracellular Ca2+ response, GKB reduced this increase. ACA attenuated the H2O2-evoked Ca2+ signal, indicating the involvement of an ACA-sensitive Ca2+-entry component. However, because ACA is not selective for TRPM2, these pharmacological findings cannot establish a TRPM2-dependent mechanism. The findings demonstrate that GKB reduces 6-OHDA-induced SH-SY5Y cell damage by supporting antioxidant defence, limiting cell death, and attenuating the enhanced oxidant-stimulated Ca2+ response.

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