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. 2022 May 9;12(8):3928–3945. doi: 10.7150/thno.70762

Figure 1.

Figure 1

The deficiency of 5-HT2B promotes the occurrence of CAC. (A) Schematic overview of the AOM/DSS model of CAC in mice. (B) The colonic polyp multiplicity and polyp load in WT (n = 9) and Htr2bΔIEC (n = 7) mice following the induction of CAC using AOM/DSS. Each data point represents a single mouse. (C) Hematoxylin-eosin (H&E) staining of representative colonic sections from WT and Htr2bΔIEC mice treated with AOM/DSS. Arrow: aggressive adenomas with invasion; asterisk: muscularis mucosa and angiogenesis. (D) Typical immunohistochemical analysis of 5-HT2B and 5-HT in colonic polyp tissues from WT and Htr2bΔIEC mice. (E) Immunohistochemical analysis of Ki-67 and cleaved caspase-3 in colonic polyp tissues of WT and Htr2bΔIEC mice. (F) The percentage of Ki-67 (n = 6) and cleaved caspase-3 (n = 5) positive cells (positive epithelial cells/total epithelial cells) in colonic polyp tissues of WT and Htr2bΔIEC AOM/DSS-treated mice. Error bars represent the mean ± SEM. Scale bars, 100 μm. ns: not significant, *P < 0.05, ***P < 0.001; unpaired Student's t-test (B, F).