Copyright
©The Author(s) 2002.
World J Gastroenterol. Apr 15, 2002; 8(2): 217-223
Published online Apr 15, 2002. doi: 10.3748/wjg.v8.i2.217
Published online Apr 15, 2002. doi: 10.3748/wjg.v8.i2.217
Figure 4 The role of procaspase 8 and procaspase 9 in JTE-522 induced apoptosis for indicated time.
4A: Effect of JTE-522 on caspase activities for indicated time. Data presented are the mean value of three separate experiments. 4B: Western blot shows the cleavage of procaspase 8 (Casp 8) and procaspase 9 (Casp 9). AGS cells were treated with JTE-522 for the indicated times. 4C: Effect of caspase inhibitor on JTE-522 induced DNA fragmentation. AGS cells were treated with: 1: control; 2: 1 mmol/L JTE-522; 3: 0.5 mmol/L JTE-522; 4: 50 μmol/L Z-VAD.fmk + 1 mmol/L JTE-522; 5: 50 μmol/L Ac-IETD-CHO + 1 mmol/L JTE-522; 6: 50 μmol/L Ac-LEHD-CHO + 1 mmol/L JTE-522 for 24 h.
- Citation: Li HL, Chen DD, Li XH, Zhang HW, Lü JH, Ren XD, Wang CC. JTE-522-induced apoptosis in human gastric adenocarinoma cell line AGS cells by caspase activation accompanying cytochrome C release, membrane translocation of Bax and loss of mitochondrial membrane potential. World J Gastroenterol 2002; 8(2): 217-223
- URL: https://www.wjgnet.com/1007-9327/full/v8/i2/217.htm
- DOI: https://dx.doi.org/10.3748/wjg.v8.i2.217