Ginkgolide B inhibits NLRP3 inflammasome activation and promotes microglial M2 polarization in Aβ-induced microglia cells.

Nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome-mediated chronic neuroinflammation plays a crucial role in the progression of Alzheimer's disease (AD), which is related to microglial activation. Using quantitative proteomic analysis, we identified 25 up-regulated and 83 down-regulated proteins in amyloid beta (Aβ)-induced BV2 cells. Among the differentiallyexpressedproteins involved in inflammation, the NLRP3 protein level increased dramatically. Ginkgolide B (GB) prevents Aβ-induced neuroinflammation and neurotoxic effects in multiple neurodegenerative disorders. However, its role in NLRP3 inflammasome-mediated neuroinflammation in AD remain unknown. We found that GB treatment ameliorated Aβ-induced pathological damages and inhibited NLRP3 inflammasome activation. Furthermore, GB enhanced the expression of M2 microglial markers and suppressed the expression of M1 microglial markers. Our findings suggest that GB treatment prevents the pathological processes of AD and suppresses neuroinflammation by inhibiting NLRP3 inflammasome activation and promoting microglial M2 polarization.