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• W2087804982 abstract "Rotenone-induced apoptosis is considered to contribute to the etiology of Parkinson's disease (PD). We try to prevent the apoptosis induced by rotenone toxicity with 50 μM myricetin, 100 μM fraxetin and 100 μM N-acetylcysteine (NAC) that protect against reactive oxygen species (ROS), on SH-SY5Y human neuroblastoma cell line. Morphological changes induced by rotenone and intracellular ROS were assessed in live SH-SY5Y dopaminergic cells by confocal microscopy using the fluorescent dyes, dihydroethidium and 2′,7′-dichlorofluorescein diacetate (DCFH-DA). DNA fragmentation was assayed as index of apoptosis. We also investigated oxidative stress parameters such as the glutathione redox status and lipid peroxidation. The exposure of the SH-SY5Y cells to rotenone 5 μM for 16 h produced severe morphological changes, DNA fragmentation and significative increases in the levels of hydrogen peroxide and superoxide anion. These increases were reduced by a 30-min pretreatment with fraxetin 100 μM or NAC 100 μM. DNA laddering produced by rotenone treatment was also inhibited by fraxetin and NAC. Treatment with 5 μM rotenone induced loss of reduced glutathione (GSH) and increased cellular levels of oxidized glutathione (GSSG). Fraxetin and NAC treatments restored glutathione redox ratio diminished after rotenone challenge and decreased the levels of lipid peroxidation. These results suggest that the natural antioxidants, such as fraxetin, may prevent the apoptotic death of dopaminergic cells induced by rotenone and mediated by oxidative stress." @default.
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• W2087804982 date "2004-05-01" @default.
• W2087804982 modified "2023-09-30" @default.
• W2087804982 title "Neuroprotective effect of fraxetin and myricetin against rotenone-induced apoptosis in neuroblastoma cells" @default.
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• W2087804982 doi "https://doi.org/10.1016/j.brainres.2004.02.065" @default.
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