Journal
MOLECULAR MEDICINE REPORTS
Volume 19, Issue 6, Pages 4890-4896Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2019.10148
Keywords
sulforaphane; PC12 cells; nuclear factor erythroid 2-related factor 2; 1-methyl-4-phenyl pyridine ion; oxidative stress; Parkinson's disease
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Funding
- National Natural Science Foundation of China [81760221, 81260211]
- National Science & Technology Fundational Resource Investigation Program of China [2018FY100900]
- Youth Project of Education Department of Jiangxi Province [151007]
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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 mu mol/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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