Isoliquiritigenin attenuates neuroinflammation in mice model of Parkinson's disease by promoting Nrf2/NQO-1 pathway

Parkinson's disease (PD) is a common neurodegenerative disease that severely affects the quality of life of patients. There is no specific drug for PD up to now. Previous studies have shown that neuroinflammation plays an important role in the pathogenesis of PD. Isoliquiritigenin (ILG) is thought to have a variety of biological activities including anti-inflammatory. However, to date, no studies have reported the role of ILG on neuroinflammation in PD in vivo. This study aimed to investigate the effect of ILG on PD in vivo and its mechanism, and to provide an experimental basis for clinical treatment of PD. Our results showed that ILG at a concentration of 20 mg/kg was effective in reducing the number of rotations in PD mice. In addition, ILG increased the expression of tyrosine hydroxylase and decreased the expression of alpha-synuclein. The results also showed that ILG reduced the expression of Iba1, IL-1 beta, IL-6, and TNF-alpha. Not only that, ILG also upregulated the expression of Nrf2 and NQO-1 in vivo. Our results suggest that ILG significantly attenuates neurological deficits in PD, and the mechanism may be through the activation of the Nrf2/NQO-1 signaling pathway to reduce neuroinflammation. Moreover, our findings provide a new therapeutic strategy for PD.