The miR-650/GCLM Axis Is Associated With Oxidative Stress and Neuroinflammation in Parkinson's Disease

Parkinson's disease (PD) is one of the common neurodegenerative diseases and is difficult to cure. The mechanisms underlying PD are incompletely understood.

This study investigated the changes in miR-650 expression in PD patients, aiming to assess its potential diagnostic value, and preliminarily explored the molecular mechanism by which miR-650 regulates oxidative damage and neuroinflammation.

The clinical data and blood samples were collected from PD patients. PD models were established in MPTP-treated mice and MPP+-treated BV2 cells. The function and molecular mechanism of miR-650 were then investigated through behavioral assessments, data analysis (such as ROC analysis and logistic regression analysis), and molecular analysis (such as Western blot, ELISA, and flow cytometry).

miR-650 was upregulated in PD and exhibited diagnostic potential. The MPTP-induced PD mouse model displayed motor dysfunction, increased accumulation of α-synuclein, enhanced oxidative stress and inflammatory response. These symptoms were effectively alleviated by inhibiting miR-650. In BV2 cells, inhibiting miR-650 reduced oxidative stress and inflammatory responses by negatively regulating GCLM.

The upregulated expression of miR-650 may have potential diagnostic value in PD. Animal and cellular experiments indicate that inhibiting miR-650 alleviates the motor disorders, oxidative stress, and inflammatory responses in PD by negatively regulating GCLM.