RESUMEN
Baicalin, a potent anti-oxidative and anti-inflammatory flavonoid compound derived from Scutellaria baicalensis, has emerged as a neuroprotective agent. However, the mechanisms by which baicalin is neuroprotective in Parkinson's disease (PD) remain unclear. In this research, α-syn/MPP+ and MPTP were used to establish PD models in BV2 cells and C57BL/6 mice, respectively. The effect and mechanism of action of baicalin in PD were investigated by Western blotting, RT-qPCR, ELISA, Immunohistochemistry (IHC) staining, Immunofluorescence (IF) staining, HPLC and methods. Results demonstrate that baicalin mitigates oxidative stress, microglia activation and inflammatory response caused by α-syn/MPP+ and MPTP. It protects against dopaminergic neuron loss and relieves motor deficits. Meanwhile, baicalin not only significantly up-regulates the expression of Nrf2 and its downstream antioxidant enzyme, but also suppresses the activation of NLRP3 inflammasome simultaneously. Notably, the beneficial effects of baicalin in PD treatment are blocked by Nrf2 knockdown. This research reveals that baicalin may exert neuroprotective effects in PD treatment by suppressing the activation of NLRP3 inflammasome and it is dependent on the Nrf2-mediated antioxidative response.
