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To investigate the effects of allicin on the growth and apoptosis induction of human gastric cancer SGC-7901 cells.Human gastric cancer cell line SGC-7901 cells were incubated with various concentration of allicin.After various periods of incubation, the proliferation of SGC-7901cells was assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide methyl thiazolyl tetrazolium (MTT) assay.The morphology of the apoptotic cell was observed under a fluorescent microscope and trasmission electron microscope.DNA fragment analysis was used to confirm the presence of apoptosis.Flow cytometry with regular propidium iodide (PI) staining was performed to analyze the cell cycle distribution of SGC-7901 cells and to assess apoptosis by annexin v-fluorescein isothiocyanate (V-FITC)/PI staining.Rh123 staining was used to detect the alteration of mitochondrial membrane potential (△ψm).The mRNA levels of Bax, Bcl-2 were further confirmed by Fluorescence quantitative PCR.The protein levels of Bax, Bcl-2 were further confirmed by Western blotting.SGC-7901 cells showed typical apoptotic morphological changes after treated with allicin (80 μg/mL) for 48 h.Cell death assay indicated that SGC-7901 cells underwent apoptosis in a dose-dependent manner induced by allicin, and the IC50 at 48h was 78±2.04 μg/mL.Allicin significantly inhibited the growth of human gastric cancer cell lines and arrested SGC-7901 cell cycle at G1 phase.In addition, allicin treatment could downregulate the protein and mRNA level of Bcl-2 and upregulate the Bax, leading to the increase in the ratio of Bax to Bcl-2 in SGC-7901 cells.Allicin is able to induce apoptosis in gastric cancer.The results suggest allicin induced apoptosis of gastric cancer cells through down-regulating Bcl-2 expression, and up-regulating Bax expression.