Resveratrol(10 μmol/L) could partially reverse the inhibition effects of DIM(30 μmol/L) on cellur proliferation. Effect of DIM on cell cycle Flow cytometric analysis revealed that DIM treatment induced changes in cell cycle distribution, with increased accumulation of SGC7901 cells in the G1 phase and compensation for this change by a decrease of cells in the S phase (Figure 4 and Table

1). Figure 4 The effect of DIM on cell cycle of SGC7901 cells. SGC7901 cells were treated with different concentrations of DIM Ruboxistaurin mw and subjected to flow cytometric analysis. The percentage of each phase is indicated in each panel. The results shown are representative of three independent experiments. Table 1 The effect of DIM on cell cycle of SGC7901 cells DIM concentration (μmol/L) Percentage of cell cycle (%) G1 G2 S 0 55.90 ± 1.48 10.5 ± 0.95 33.63 ± 0.55 10 57.20 ± 0.36* 9.10 ± 0.3 33.70 ± 0.53 20 61.03 ±1.53* 8.17 ± 0.68 30.77 ± 0.97* 30 61.97 ± 0.32* 9.83 ± 0.32 28.23 ± 0.60* 40 62.77 ± 1.46* 9.13 ± 0.91 28.10 ± 0.56* 50 73.03 ± 4.05* 9.17 ± 1.51 18.07 ± 0.57* *p < 0.05, vs the control. Effect of DIM on cell apoptosis 48 h after DIM treatment, the changes of cell apoptosis were observed by flow cytometric analysis. Compared to the control group, cell apoptosis GW786034 solubility dmso was induced at concentrations of 20 to 50 μmol/L, and the apoptosis

rate increased in a dose-dependent manner. These results showed that DIM could induce cell apoptosis Mirabegron in SGC7901 cells (Figure 5 and Table 2). Figure 5 The effect of DIM on apoptosis of SGC7901 cells. SGC7901 cells were treated with different concentrations of DIM and subjected to flow cytometric analysis. The results shown are representative of three independent experiments. Table 2 The effect of DIM on apoptosis of SGC7901 cells DIM concentration (μmol/L) Apoptosis rate (%) 0 4.18 ± 0.23 10 4.81 ± 0.42 20 6.07 ± 0.33* 30 7.23 ± 0.78# 40 7.39 ± 1.08# 50 9.14 ± 0.32# *p < 0.05, #p < 0.01vs the control. Discussion Our previous work found that the expression of AhR was significantly up-regulated in gastric cancer, and may be involved in the early

stage of gastric carcinogenesis, regulation of the AhR pathway may have a potential role in the treatment of gastric cancer. We hypothesized that AhR ligands may be utilized for gastric cancer therapy. Then our futher studies showed that TCDD, a potent AhR agonist, could supresse the growth of gastric cancer cell AGS in a dose- and time-depengent manner via induction of growth arrest at the G1-S phase [9]. But TCDD itself is carcinogenic, it induces a broad spectrum of biological learn more responses, including induction of CYP1A1, disruption of normal hormone signaling pathways, reproductive and developmental defects, immunotoxicity, liver damage, wasting syndrome, and cancer [18], so non-toxic or low-toxic selective AhR modulators maybe served as possible agents for gastric cancer.