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)_1-42-induced BV2 cells. Among the differentially expressed proteins 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_1-42-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.

核苷酸结合寡聚化结构域 (NOD) 样受体蛋白 3 (NLRP3) 炎症小体介导的慢性神经炎症在与小胶质细胞激活有关的阿尔茨海默病 (AD) 的进展中起关键作用。_{使用定量蛋白质组学分析，我们在β淀粉​​样蛋白 (Aβ) 1-42}诱导的 BV2 细胞中鉴定了 25 种上调和 83 种下调的蛋白质。在与炎症有关的差异 表达 蛋白中，NLRP3 蛋白水平显着增加。Ginkgolide B (GB) 在多种神经退行性疾病中预防 Aβ 诱导的神经炎症和神经毒性作用。然而，它在 AD 中 NLRP3 炎症小体介导的神经炎症中的作用仍然未知。我们发现 GB 治疗改善了 Aβ _1-42-诱导的病理损伤并抑制 NLRP3 炎症小体的活化。此外，GB 增强了 M2 小胶质细胞标志物的表达并抑制了 M1 小胶质细胞标志物的表达。我们的研究结果表明，GB 治疗通过抑制 NLRP3 炎性体激活和促进​​小胶质细胞 M2 极化来预防 AD 的病理过程并抑制神经炎症。