Abstract: Objective To observe whether DJ-1 could relieve the mitochondrial dysfunctions and cell apoptosis in MN9D cellafter rotenone exposure. Methods MN9D cell lines was exposed to rotenone (100nM) for 24h after transfected with human mutant (L166P) or wild-type (WT) DJ-1.Cells were divided into Co, WT-DJ-1 (WT), L166P-DJ-1 (L166P) group. Cell viability was measured by MTT, and mitochondrial membrane potential (ΔΨm) by JC-1 and cell apoptosis by AnnexinⅤ+PI and TUNLE staining. Results Cell viability of Co group reduced to 48.2%±6.4%, and WT group was 78%±3.7% (P<0.05), there was not statistical difference between Co group and L166P group. Overexpression of WT-DJ-1 could partly rescue ΔΨm which was reduce after rotenone exposure (P<0.05), however, overexpression of L166P exacerbated the reduce of ΔΨm. And cell death in WT group was 5.4% and 9.7% after rotenone exposure for 12h or 24h respectively, accordingly 10.9% and 23.2% in Co group (P<0.05). There was not statistic difference between Co group and L166P group. TUNEL staining showed the similar trend. Conclusion Overexpression WT-DJ-1 could relieve the cell injury after rotenone exposure and dull the mitochondrial dysfunction. However, L166P had not the protective role after rotenone exposure.

Key words: Parkinson’s disease, DJ-1, rotenone, apoptosis, mitochondrial dysfuction