Skip to main content
. 2018 Mar 23;9(22):15847–15859. doi: 10.18632/oncotarget.24627

Figure 1. Analysis of Gpx2 expression by immunohistochemistry using a rat bladder carcinogenesis model.

Figure 1

(A-D) HE staining (A, C) and representative immunohistochemistry for Gpx2 (B, D) in normal bladder epithelium obtained from the non-treated group (A, B) and BBN + 0.05% PEITC-treated (C, D) rats. (E, F) HE staining (E) and representative immunohistochemistry for Gpx2 (F) in PNHP of the bladder obtained from BBN + 0.05% PEITC-treated rats. (G, H) HE staining (G) and representative immunohistochemistry for Gpx2 (H) in papillary pure UC of the bladder obtained from BBN + 0.05% PEITC-treated rats. (I, J) HE staining (I) and representative immunohistochemistry for Gpx2 (J) in UC with squamous cell differentiation (SqD) of the bladder obtained from BBN + 0.05% PEITC-treated rat. (K) Quantification of intensity of Gpx2 expression in normal epithelium. In BBN + PEITC-treated rats, the expression level of Gpx2 was significantly increased as compared to that in the control non-treated group (Control). Mean ± SD; *p<0.05. (L) Quantification of intensity of Gpx2 expression in the BBN + 0.05% PEITC-treated group. The expression level of Gpx2 was significantly increased in PNHP, UC, and SCC as compared to normal epithelium. In addition, the expression level of Gpx2 was the highest in UC with SqD. Mean ± SD; *p<0.05, ***p<0.001, ****p<0.0001. Nuclei were counterstained with hematoxylin.