| ObjectiveTo assess the inhibition of proliferation and the induction of apoptosis ofgallium nitrate, cisplatin and combination with two drugs on human gastric(BGC823)cells. we investigated the expression of Bcl-2, Bax and Caspase-3and the possible mechanism in gallium nitrate-induced gastric cancer BGC823cells apoptosis and inhibition of proliferation. Our study will provide a new wayof oral drugs for therapy of gastric cancer.MethodsThe human gastric cancer cell line BGC823was cultured and treated withdrugs, Cells were divided into four groups, control, gallium nitrate group,cisplatingroup and combination group. Cell apoptosis was determined by flowcytometry.cell proliferation was measured using MTT assay. Expression of Bcl-2,Bax and Caspase-3were analyzed by Western blot.Results1, Gastric cancer cell line BGC823was treated with different concentrationsof gallium nitrate, and MTT assay showed that gallium nitrate inhibited BGC823cell proliferation in time and dose-dependent manner.The percentage ofapoptosis cells were statistical significance compare with the untreated controlgroup.2, Apoptosis of cells was examined by flow cytmetry, and the results showed that cells treated with gallium nitrate, cisplatin and combination with thetwo drugs resulted in a significant increase (P<0.05)in apoptosis. Thepercentage of apoptosis in combination group was the highest than others.3, The expression of Bcl-2protein was downregulated in gallium nitrategroup, cisplatin group and combination group compare with control. Bax andaspase-3protein were activated in gallium nitrate group and combination groupcompare with control, but there is no significant differences in cisplatin group.Conclusions1, Effects of gallium nitrate on cell proliferation and apoptosis in humangastric cancer cells had no significant difference with cisplatin, but there werestatistical significance in expression of Bax and Caspase compare with cisplatin.2, gallium nitrate and cisplatin affect gastric cells in time anddose-dependent manner.3, gallium nitrate down-regulated the expression of Bcl-2and up-regulatedthe expression of Bax and Caspase-3may be involved in its mechanism. |