BackgroundAlbiflorin isolated from Paeoniae Alba Radix can cross the blood-brain barrier (BBB) and possesses analgesia, anticonvulsant, anti-inflammatory, and hepatoprotective properties. This study investigates albiflorin functions and related mechanisms in Parkinson's disease (PD) pathogenesis.MethodsCellular and animal models of PD were constructed. Cell viability and apoptosis were detected by CCK-8 assays. Levels of Iba-1 and TH were measured by immunofluorescence staining, western blotting, and immunohistochemistry staining. Levels of pro-inflammatory mediators and pathway-related genes were measured by western blotting and RT-qPCR. Locomotor activity of mice was examined by open field test, rod climbing test, and rod rotating test.ResultsFor in vitro analysis, albiflorin inhibited LPS-induced microglial activation and neuroinflammation. Additionally, albiflorin inactivated NF-kappa B and MAPK pathways in LPS-treated BV2 cells. Moreover, albiflorin attenuated neurotoxicity mediated by LPS-stimulated microglia. For in vivo analysis, albiflorin improved MPTP-induced locomotor activity deficits and reduced MPTP-induced dopaminergic neuron loss. In parallel, albiflorin inhibited activated microglia-mediated neuroinflammation in MPTP-treated mice.ConclusionAlbiflorin mitigates neuronal apoptosis and improves behavioral impairments in MPTP-induced PD mouse model through inhibition of activated microglia-mediated neuroinflammation via the NF-kappa B and MAPK pathways.