Molecular Medicine Reports · 2019 · 29 citations · 43 references
Life SciencesPharmacologyToxicologyApoptosisMechanisms Of ToxicityNeurochemistryAntioxidant DefenseCellular ToxicologyNeuroprotectionOxidative Damage To BiomoleculesOxidative Stress MechanismsReactive Oxygen SpeciesAntioxidant PropertiesCell Viability AssaysHeme Oxygenase-1Nrf2-mediated Cytoprotective SignalingNrf2-mediated ResponsesOxidative Stress InjuryOxidative Stress ToxicityOxidative Stress-induced Cell Death
The aim of this study was to investigate the protective effect of sulforaphane (SFN) on 1‑methyl‑4‑phenyl pyridine ion (MPP+)‑induced cytotoxicity and to investigate its possible mechanisms. METHODS: PC12 cell toxicity induced by MPP+ served as a cell model of Parkinson's diseases. The cell culture + experiments were divided into four groups based on the different treatments, namely, vehicle control, SFN, MPP+ and SFN pretreatment plus MPP+. Cell viability and apoptosis were examined by MTT assay and flow cytometry, respectively. Expressions of nuclear factor erythroid 2‑related factor 2 (Nrf2), heme oxygenase 1 (HO‑1) and nicotinamide quinone oxidoreductase 1 (NQO1) were detected using western blotting. RESULTS: MPP+ reduced the survival rate of PC12 cells in a dose‑ and time‑dependent manner. After 24‑h treatment with 500 µmol/l MPP+, the survival rate of PC12 cells decreased to 58.2±0.03% of that in the control groups. Under the same conditions MPP+ resulted in significant apoptosis of PC12 cells (apoptosis rate: 30.4±0.6%). However, SFN pretreatment significantly attenuated the cell damage induced by MPP+. Furthermore, it was demonstrated that SFN reversed the reduction of Nrf2, HO‑1 and NQO1 expression induced by MPP+. CONCLUSION: SFN may protect PC12 cells from MPP+‑induced damage via activating the Nrf2‑ARE (antioxidant responsive element) pathway.
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Changjiang Xu, Mou‐Tuan Huang, Guoxiang Shen et al. · Cancer Research · 2006 · 382 citations · Full text
Medicine, Oncology, Pharmacology +17