Luteolin alleviates oxygen-glucose deprivation/reoxygenation-induced neuron injury by regulating NLRP3/IL-1β signaling

We aimed to investigate the protective effect of luteolin against neuron injury induced by oxygen-glucose deprivation/reoxygenation (OGD/R), and to further elucidate the roles of NLRP3 in luteolin-mediated regulation of neuron injury. Using Schwann (SW) 10 cells, an OGD/R-induced neuron injury model was established, and six experimental groups were designated. Subsequently, cell viability and apoptosis were respectively detected by cell counting kit 8 and flow cytometry. Reactive oxygen species (ROS) levels were measured via flow cytometry with a ROS assay kit. Moreover, the expression of interleukin (IL)-6, IL-1β, NLRP3, and MMP9 was examined by real-time quantitative PCR and Western blot. Compared with control cells, OGD/R significantly reduced cell viability and increased apoptosis, ROS levels, and the mRNA levels of IL-6 , IL-1β , NLRP3 , and MMP9 . Luteolin significantly enhanced OGD/R-induced cell viability and alleviated apoptosis in SW10 cells ( P < 0.05). Additionally, luteolin suppressed ROS levels, along with the expression of IL-1β, IL-6, NLRP3, and MMP9 induced by OGD/R. Furthermore, BMS-986299 significantly decreased the cell viability and increased the expression of inflammatory factors in OGD/R-induced SW10 cells treated with luteolin. This inhibitory effect was reversed by NLRP3 knockdown. In conclusion, luteolin may exert a protective effect on OGD/R-induced nerve injury by inhibiting the NLRP3/IL-1β signaling pathway.