Albiflorin ameliorates neuroinflammation and exerts neuroprotective effects in Parkinson's disease models

Background: Albiflorin 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.

Methods: Cellular 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.

Results: For in vitro analysis, albiflorin inhibited LPS-induced microglial activation and neuroinflammation. Additionally, albiflorin inactivated NF-κB 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.

Conclusion: Albiflorin mitigates neuronal Apoptosis and improves behavioral impairments in MPTP-induced PD mouse model through inhibition of activated microglia-mediated neuroinflammation via the NF-κB and MAPK pathways.