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. 2020 Nov 5;11(3):857–880. doi: 10.1016/j.jcmgh.2020.10.015

Figure 4.

Figure 4

H pylori promotes gastric epithelial cell senescence via CXCR2 signaling. Part B. (A) qPCR and (B) Western blot showing changes in the expression of CXCR2 and its ligands in the DNA damage–induced senescence model (means ± SD, unpaired t test). Two independent replicates were performed. (C) CXCR2 expression was evaluated using Western blot analysis after AGS and GES-1 cells were transfected with lentivirus encoding CXCR2. (D) SA-β-gal and BrdU staining showing senescent cells. Cells were transfected with lentivirus encoding CXCR2 or a control vector and then exposed to 5 Gy X-ray, followed by culture for another 5 days before staining (means ± SD, unpaired t test). Scale bar: 50 μm. (E) Western blot analysis detecting CXCR2 expression in AGS and GES-1 cells transfected with CXCR2 small interfering (si)RNA or negative control sequences. (F) SA-β-gal and BrdU staining showing senescent cells. Cells were exposed to 5 Gy X-ray after transfection and then cultured for another 5 days before staining (means ± SD, unpaired t test). Scalebar: 50 μm. (G) AGS cells were first transfected with CXCR2 siRNA or treated with SB225002 and then exposed to 5 Gy X-ray. After that, the cells were cocultured with PBS or PMSS1. SA-β-gal staining and BrdU labeling were performed 5 days later (means ± SD, unpaired t test). Scale bar: 20 μm. All of the results are representative of 3 independent experiments. ∗P < .05. ∗∗P < .01. ∗∗∗P < .001. DMSO, dimethyl sulfoxide; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; NC, negative control.