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. 2021 Nov 22;10(11):1219. doi: 10.3390/biology10111219

Figure 7.

Figure 7

Terretonin (TE) suppressed the LPS-induced activation of NF-κB/NLRP3 signaling and its downstream pro-inflammatory markers in the lung. (I) (A) Gene expression; (B) level of NF-κB; (C) gene expression of NLRP3; (D) gene expression of caspase-1. (II) Immuno-expression of NF-κB protein: (A,B) lung sections of both the control and TE 40 groups, showing minimal cytoplasmic brownish staining; (C) LPS group showing marked nuclear and cytoplasmic brown immunostaining of inflamed lung tissue; (D) TE 20 + LPS and (E) TE 40 + LPS groups exhibiting marked improvement with moderate to minimal nuclear and cytoplasmic brown staining; NF-ĸB immunostain ×400, scale bar 25 µm; (F) % of immunopositive cells among different groups. (III) (A–D) Gene expression of iNOS, TNF-α, IL-1β, and IL-6; (E–H) levels of NOx, TNF-α, IL-1β, and IL-6. Data are the mean ± SE (n = 8). * p < 0.05, ** p < 0.01, *** p < 0.001 vs. control group; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. LPS group (one-way ANOVA followed by Tukey’s Kramer multiple comparisons test).