ABSTRACT
AIM To study the effects of vitamin E succinate (VES) on the cell growth and the DNA synthesis of human gastric carcinoma cell (SGC-7901). METHODS The growth curve was determined with counting viable cell numbers. The colony formations were counted with Giemsa dye staining. The cell cycle was analyzed using flow cytometry (FCM) and the DNA synthesis was observed with the 3H-TdR incorporation method. RESULTS VES could inhibit the growth and colony formation of SGC-7901 cells. Growth curve display：after SGC-7901 cells were treated with 5 mg*L-1、10 mg*L-1 and 20 mg*L-1 VES for seven days, the inhibition rate are 41.2%、98.3% and 100%, respectively. The colony formation of SGC-7901 cell at 24 h was inhibited 6.7%、50.4%、87.2%, and at 48 h was 24.7%、73.4%、100%, respectively. FCM analysis revealed that VES could decrease the percentage of cells in G2-M phase after treated 48 h in a dose-dependent manner, while increase the percentage of cells in S pheise. The assays of 3H-TdR incorporation into DNA showed obvious inhibition dose-dependently after exposure to VES for 48 h. CONCLUSION VES could inhibit gastric carcinoma cell growth by arresting DNA synthesis in vitro.
ABSTRACT
AIM To study the effects of vitamin E succinate (VES) on the cell growth and the DNA synthesis of human gastric carcinoma cell (SGC 7901). METHODS The growth curve was determined with counting viable cell numbers. The colony formations were counted with Giemsa dye staining. The cell cycle was analyzed using flow cytometry (FCM) and the DNA synthesis was observed with the 3H TdR incorporation method. RESULTS VES could inhibit the growth and colony formation of SGC 7901 cells. Growth curve display:after SGC 7901 cells were treated with 5 mg?L -1 、10 mg?L -1 and 20 mg?L -1 VES for seven days, the inhibition rate are 41 2%、98 3% and 100%, respectively. The colony formation of SGC 7901 cell at 24 h was inhibited 6 7%、50 4%、87 2%, and at 48 h was 24 7%、73 4%、100%, respectively. FCM analysis revealed that VES could decrease the percentage of cells in G 2 M phase after treated 48 h in a dose dependent manner, while increase the percentage of cells in S pheise. The assays of 3H TdR incorporation into DNA showed obvious inhibition dose dependently after exposure to VES for 48 h. CONCLUSION VES could inhibit gastric carcinoma cell growth by arresting DNA synthesis in vitro .