Research ReportAutophagy-related protein expression in the substantia nigra and eldepryl intervention in rat models of Parkinson׳s disease

●Autophagic activity was activated in the substantia nigra of rat models of Parkinson׳s disease.●Autophagy participates in the onset and development of Parkinson׳s disease.●Eldepryl exerts therapeutic effect on Parkinson׳s disease possibly by inhibiting the nerve cell autophagy.●This provides a novel pathway and target for drug treatment for Parkinson׳s disease.

Autophagy has been shown to participate in the pathogenesis of Parkinson׳s disease (PD), but its precise mechanism remains poorly understood. This study observed autophagy, autophagy-related protein Beclin1 and microtubule-associated protein 1 light chain 3 (LC3) expression in substantia nigra, and eldepryl effects on their expression, as well as explored autophagy effects on the onset of PD and the mechanism of action of eldepryl on PD in rat models. Models of PD were established by subcutaneous injection of rotenone through back of the neck. Results indicated that Beclin1, LC3 protein expression and LC3II/LC3I ratio were higher in substantia nigra of rats in the model group compared with the control group. Beclin1, LC3 protein expression and LC3II/LC3I ratio were higher at 8 days than that at 4 days in the model group, showing significant differences. Beclin1, LC3 protein expression and LC3II/LC3I ratio were lower in the rat substantia nigra of the eldepryl group than in the model group. Beclin1, LC3 protein expression and LC3II/LC3I ratio were lower at 8 days than at 4 days in the eldepryl group, showing significant differences. Results suggested that autophagy plays a key role in the onset of PD. Eldepryl exerts therapeutic effects on PD by inhibiting autophagy of nerve cells in substantia nigra of rat models of PD.