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. Author manuscript; available in PMC: 2020 Jun 29.

Published in final edited form as: Helicobacter. 2008 Dec;13(6):506–517. doi: 10.1111/j.1523-5378.2008.00646.x

Fig. 2. — H. pylori-induced apoptosis in gastric cells involves the activation of procaspase-8 with cleavage of nuclear lamins and PARP. AGS cells were overlaid with culture medium containing H. pylori (at 100 bacteria per gastric cell, strains J117, cagA+) for 24 hours. (A) Cytoplasmic and nuclear proteins were run on SDS-PAGE and probed for anti-human caspase-8. Presence of activated caspase-8 protein observed in AGS cells treated with H. pylori. HCT116 and AGS cells treated with NaB or Staurosporine were used as positive controls. (B) Immunoblot showing the presence of cleaved nuclear lamin B fragments in cells treated with H. pylori but not in untreated AGS or in cells treated with staurosporine. (C) Cleaved PARP protein fragments observed in total protein lysates of H. pylori-treated cells but not in untreated controls. Results in A-C are representative of data obtained from two or more separate experiments.

Fig. 2. — H. pylori-induced apoptosis in gastric cells involves the activation of procaspase-8 with cleavage of nuclear lamins and PARP. AGS cells were overlaid with culture medium containing H. pylori (at 100 bacteria per gastric cell, strains J117, cagA+) for 24 hours. (A) Cytoplasmic and nuclear proteins were run on SDS-PAGE and probed for anti-human caspase-8. Presence of activated caspase-8 protein observed in AGS cells treated with H. pylori. HCT116 and AGS cells treated with NaB or Staurosporine were used as positive controls. (B) Immunoblot showing the presence of cleaved nuclear lamin B fragments in cells treated with H. pylori but not in untreated AGS or in cells treated with staurosporine. (C) Cleaved PARP protein fragments observed in total protein lysates of H. pylori-treated cells but not in untreated controls. Results in A-C are representative of data obtained from two or more separate experiments.