Ming-wei Chen1, Lan Yang, Lei Ni, Chen Huang. 1. Department of the Respiratory, the First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Xi'an 710061, China.
Abstract
OBJECTIVE: To assess the effect of 20(R)-Rg3 on the inhibition of angiogenesis of lung cancer and explore its role in the change of endogenous VEGF secreted by A549 tumor cells themselves. METHODS: A549 tumor cells were cultured with different concentrations of 20(R)-Rg3(10(-7) mol/L, 10(-6) mol/L, 10(-5) mol/L and 10(-4), mol/L), the VEGF contents were detected by ELASA method after 24 h, 48 h and 72 h. Cellular proliferation was detected by MTT method, and apoptosis was detected with flow cytometry. RESULTS: It was found that Rg3 had no significant inhibitory effect on the proliferation of A549 cells. The apoptosis rate was 29.8% after the cells being interfered with Rg3 at 3 x 10(-5) mol/L for 120 h. The levels of VEGF in the groups of Rg3 at 10(-5) mol/L and 10(-4) mol/L were lower than that in the contrast group (P < 0.05). The level of VEGF in the group of 10(-4) mol/L was lower than that in the group of 10(-7) mol/L and group of 10(-6) mol/L, and it was lower after 72 h of interference than that after 24 h and 48 h of interfernce. CONCLUSION: With the action of 20 (R)-Rg3, the level of VEGF secreted by A549 tumor cells themselves declined; the apoptosis of A549 tumor cells increased, especially at higher concentration and longer action time of Rg3. This might be one of the antiangiogenesis mechanisms of 20(R)-Rg3.
OBJECTIVE: To assess the effect of 20(R)-Rg3 on the inhibition of angiogenesis of lung cancer and explore its role in the change of endogenous VEGF secreted by A549 tumor cells themselves. METHODS:A549 tumor cells were cultured with different concentrations of 20(R)-Rg3(10(-7) mol/L, 10(-6) mol/L, 10(-5) mol/L and 10(-4), mol/L), the VEGF contents were detected by ELASA method after 24 h, 48 h and 72 h. Cellular proliferation was detected by MTT method, and apoptosis was detected with flow cytometry. RESULTS: It was found that Rg3 had no significant inhibitory effect on the proliferation of A549 cells. The apoptosis rate was 29.8% after the cells being interfered with Rg3 at 3 x 10(-5) mol/L for 120 h. The levels of VEGF in the groups of Rg3 at 10(-5) mol/L and 10(-4) mol/L were lower than that in the contrast group (P < 0.05). The level of VEGF in the group of 10(-4) mol/L was lower than that in the group of 10(-7) mol/L and group of 10(-6) mol/L, and it was lower after 72 h of interference than that after 24 h and 48 h of interfernce. CONCLUSION: With the action of 20 (R)-Rg3, the level of VEGF secreted by A549 tumor cells themselves declined; the apoptosis of A549 tumor cells increased, especially at higher concentration and longer action time of Rg3. This might be one of the antiangiogenesis mechanisms of 20(R)-Rg3.