Fig. 5

Inhibition of NLRP3 inflammasome by EA stimulus was α7nAChR–Dependent. a α7nAChR antagonist reversed the inhibition of NLRP3 inflammasome by EA stimulus. Representative western immunoblotting analysis of NLRP3, Caspase-1, GSDMD and IL-1β (n = 4). Compared with EA + MCAO group, the expression of NLRP3, procaspase-1, Cl.Caspase-1, GSDMD, GSDMD-N, proIL-1β and mature IL-1β were increased in α-BGT + EA + MCAO group. **P < 0.01, ***P < 0.001 vs. Sham group, ^##P < 0.01, ^###P < 0.001 vs. MCAO group, ^&&P < 0.01, ^&&&P < 0.001 vs. EA + MCAO group. b α7nAChR agonist mimicked the inhibition of NLRP3 inflammasome by EA stimulus. Representative western immunoblotting analysis of NLRP3, Caspase-1, GSDMD and IL-1β (n = 4). Comparison with MCAO groups showed that intraperitoneal injection of PHA-543,613 down-regulated the levels of NLRP3, procaspase-1, Cl.Caspase-1, GSDMD, GSDMD-N, proIL-1β and mature IL-1β. **P < 0.01, ***P < 0.001 vs. Sham group, ^#P < 0.05, ^##P < 0.01, ^###P < 0.001 vs. MCAO group