Celastrol alleviates esophageal stricture in rats by inhibiting NLR family pyrin domain containing 3 activation

Figure 2 NLR family pyrin domain containing 3 associated inflammatory mediators in the endoscopic submucosal dissection resection bed. A: Tissue acquisition site in the post-endoscopic submucosal dissection (ESD) esophagus. Arrowhead: The ESD resection bed; Arrow: The normal esophageal mucosa; B: mRNA levels of NLR family pyrin domain containing 3 (NLRP3), interleukin (IL)-1β, and IL-18 (presented as the mean ± SD). Control: Tissues from normal esophageal mucosa; ESD: Tissues from the resection bed. Statistical analysis was performed using the Wilcoxon signed-rank test, ^aP = 0.009; ^bP = 0.02; C: Immunohistochemistry (IHC) of NLRP3 in the post-ESD resection bed: Vascular endothelial cells, myocytes, and fibroblasts (arrows). Scale bar = 50 μm; D: IHC of vimentin in human tissues from post-ESD esophageal stricture. Scale bar = 100 μm; E: Dual labeling for NLRP3 and vimentin was performed in human tissues from the resection bed. Scale bar = 20 μm. ESD: Endoscopic submucosal dissection; IL: Interleukin; NLRP3: NLR family pyrin domain containing 3.