Fig 2: NF-κB signaling pathway was involved in the ameliorative effect of NLRP3-KO on lung injury. (a) Representative western blot bands for p65, p-p65, ASC, CL-Cas1, IL-1β, and IL-18. (b ~ f) Quantification of ASC/GAPDH, CL-Cas1/GAPDH, IL-1β/GAPDH, IL-18/GAPDH, and p-p65/GAPDH, respectively. The data are presented as the mean ± SEM. n = 5 per group. AP < 0.05 vs. Sham; BP < 0.05 vs. WT.

Fig 3: The circ_0004951/miR-93-5p/ NLRP3 axis regulates HG-induced pyroptosis in HK2. LDH release in each group (A). Caspase-1 activity in each group (B). ELISA results showing expression levels of IL-1ß and IL-18 in each group (C,D). HG, high glucose; HK2, human renal tubular epithelial cell line; LDH, lactate dehydrogenase. Values are expressed as mean ± SD. *p < 0.05 vs. control.

Fig 4: Administration of Rux reduced NLRP3 inflammasome activation in HT22 cells after OGD/R. (A) Representative western blots showing NLRP3, ASC, CL-caspase-1, IL-1ß and IL-18 at the protein level. (B–F) Quantification results of NLRP3, ASC, CL-caspase-1, IL-1ß and IL-18 expression at the protein level. Means ± SD. n = 5/group. aP < 0.01 versus control; bP < 0.05 versus OGD/R + vehicle; cP < 0.05 versus OGD/R + LPS.

Fig 5: Serum levels of IL-1b and IL-18 in systemic lupus erythematosus (SLE) patients as examined by ELISA. Serum IL-1b and IL-18 levels were higher in the SLE group than in the healthy control group, and the expression of IL-1b and IL-18 was decreased after treatment (continuous methylprednisolone treatment; 40 mg/day for 2 weeks). SLE + BT: SLE patients before treatment; SLE + AT: SLE patients after treatment; IL-1b (a); IL-18 (b).*p < 0.05, #p > 0.05, as determined by the t-test