Gastric Cancer
Copyright ©2007 Baishideng Publishing Group Co.
World J Gastroenterol. Jul 28, 2007; 13(28): 3824-3828
Published online Jul 28, 2007. doi: 10.3748/wjg.v13.i28.3824
Figure 1
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Figure 1 Inhibition of the proliferation of SGC-7901 cells by NOChR. aP < 0.05 vs treatment with ChR.
Figure 2
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Figure 2 Induction of the apoptosis of SGC-7901 cells by NOChR. aP < 0.05 vs vehicle; bP < 0.01 vs vehicle.
Figure 3
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Figure 3 DNA ladder assay showing NOChR-induced apoptosis of SGC-7901 cells. Lane 1: DNA marker; lane 2: Control; lane 3: 20 μmol/L NOChR (24 h); lane 4: 20 μmol/L NOChR (48 h); lane 5: 20 μmol/L NOChR (72 h); lane 6: 20 μmol/L NOChR plus 10 μmol/L GW9662 (24 h); lane 7: 20 μmol/L NOChR plus 10 μmol/L GW9662 (48 h); lane 8: 20 μmol/L NOChR plus 10 μmol/L GW9662 (72 h).
Figure 4
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Figure 4 Western blot analysis showing regulation of PPARγ (A), Bcl-2 (B) and Bax (C) protein expressions in SGC-7901 cells by NOChR (mean ± SD, n = 3).
Figure 5
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Figure 5 PPARgamma antagonist GW9662 blocked the effects of NOChR on Bax and Bcl-2 protein expression in SGC-7901 cells. A: Bax; B:Bcl-2. SGC-7901 cells were pretreated with 10 μmol/L GW9662 for 30 min,then exposed to 5, 20 μmol/L NOChR for 24 h respectively (Western blot, mean ± SD, n = 3).