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. 2019 Oct 3;18:801–814. doi: 10.1016/j.omtn.2019.08.028

Figure 1.

Figure 1

LPS-Induced ALI Exhibits Activated NLRP3 Inflammasome and Inflammation of Alveolar Macrophages in LPS-Induced ALI Is Inhibited with the Silencing of NLRP3

(A) Protein expression levels of NLRP3, caspase-1, ASC, IL-1β, IL-18, and Cle-GSDMD in NR8383 cells treated with F-12K culture medium or LPS as detected by western blot analysis. (B) Expression levels of proinflammatory factors (TNF-α, IL-6, IL-1β, and IL-18) and anti-inflammatory factor IL-10 in NR8383 cells treated with F-12K culture medium or LPS as detected by ELISA. (C) Protein expression levels of NLRP3, caspase-1, ASC, IL-1β, IL-18, and Cle-GSDMD in LPS-exposed NR8383 cells following transfection with sh-NLRP3 or sh-NC as measured by western blot analysis. (D) Expression levels of proinflammatory factors (TNF-α, IL-6, IL-1β, and IL-18) and anti-inflammatory factor IL-10 in LPS-exposed NR8383 cells following transfection with sh-NLRP3 or sh-NC as measured by ELISA. (E) Pyroptosis of LPS-exposed NR8383 cells following transfection with sh-NLRP3 or sh-NC, as determined by PI/Hoechst 33342 double staining. *p < 0.05 versus NR8383 cells treated with F-12K culture medium; #p < 0.05 versus LPS-exposed NR8383 cells transfected with sh-NC. An unpaired t test was used to analyze data expressed as mean ± SD between two groups if the data conformed to normal distribution and homogeneity of variance. Data among multiple groups were compared using one-way ANOVA followed by Tukey’s post hoc test. The experiment was repeated three times.