Abstract
O bjective: To investigate the mechanism of miR-24 in dopaminergic neuron injury in Parkinson’s disease (PD). M ethods: In vivo and in vitr o PD models were established using rotenone. Rats underwent behavioral assessment using an open field test and a rotarod test. MN9D cell viability was measured using an MTT assay. The interaction between miR-24 and DJ-1 was investigated using a dual-luciferase reporter assay. R esults: MiR-24 expression was upregulated in the brain tissues of PD rats and in rotenone-induced MN9D cells, while DJ-1 expression, the LC3-II/LC3-I ratio, and the protein level of Beclin 1 were downregulated. Rotenone reduced MN9D cell viability and interfering with miR-24 lessened its inhibition effect. Interfering with miR-24 upregulated the LC3-II/LC3-I ratio and the protein level of Beclin 1 by increasing DJ-1 expression and then relieved rotenone-induced dopaminergic neuronal cell injury. These findings were confirmed by the PD rat model. C onclusion: Interfering with miR-24 alleviates rotenone-induced dopaminergic neuron injury via enhancing autophagy by increasing DJ-1 expression. K eywords: Parkinson’s disease, autophagy, miR-24, DJ-1, dopaminergic neuron
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