Abstract: Objective To explore the protective effect of DJ-1 on MN9D cells and its mechanisms. Methods Transiently transfected wild type DJ-1 into MN9D cells. The MN9D cell viability and cell apoptosis level were observed by MTT assay and flow cytometry, respectively. The numbers of LC3-positive puncta were observed by confocal images. The ratio of LC3II to LC3I was detected via Western blot. Results DJ-1 overexpressing could attenuate decreased cell viability induced by rotenone treatment (P<0.05). The increased of apoptosis caused by rotenone was diminished by overexpression of DJ-1 (P<0.05). Overexpressing of DJ-1 could increase the numbers of LC3 positive puncta(P<0.001) and increase the ratio of LC3II to LC3I (P<0.001) in MN9D cells treated with rotenone. Giving 3-MA could make the numbers of LC3 positive puncta down to the basal level and reduce the ratio of LC3-II/I (P<0.05). Meanwhile, giving autophagy inhibitor 3-MA, the protective effects of DJ-1 on MN9D cells were disappeared. Conclusion DJ-1 upregulated the level of autophagy can relieve the toxin caused by rotenone in MN9D cells.

Key words: autophagy, MN9D cells, rotenone, 3-MA