| Objective: To study the effect of the nonsteroidal anti-inflammatory drugs (NSAIDs) indomethacin on the proliferation and apoptotsis of gastric adnocarcinoma cell BGC-823 and try to expound the mechanism of it's anti-cancer.Methods: This study was carried out on culture of human gastric adnocarcinoma cell line BGC-823. Various concentration of indomethacin (12.5uM, 25uM, 50uM,100uM ) were added and incubated. Cell proliferation was detected with MTT colorimetric assay; cell apoptosis, cell cycle, and the expression of VEGF were detected by flow cytometry and electron microscopy.Results: Indomethacin could inhibit BGC-823 cells proliferation,increase apoptosis and assume dose-time-dependent. The duration lowest inhibition rate produced by indomethacin in BGC-823 cells was l%,the highest inhibition rate was 28.49%.After incubation with indomethacin for 24h, the most highest apoptosis rate of BGC-823 comparing with those of the control was 17.1%±1.35% vs 2.94%±1.01%.(P<0.05) After treated by indomethacin (100uM) for different time, there were different apoptosis rate, when treated for 3h,the apoptosis ratewas 3.25%,for 24h the apoptosis rate was 19.53%.Moreover the primitive effect assume alive cell apoptosis ,but the anaphase effect assume cell death. We further detect the effect of cell cycle produced by indomethacin. The event was indomethacin could make cell cycle arrest in G0/G1 phase. Besides indomethacin could down-regulation the expression of VEGF in BGC-823 and strengthen the effect of 5-FU for BGC-823.Conclusion: Indomethacin can inhibit the proliferation of BGC-823 cells. This effect maybe effectuation by indomethacin arrest cell cycle, which relating to indomethacin could probably up-regulation P27kip1. Furthermore indomethacin can prohibit tumor metastasis by down-regulation the expression of VEGF. With it's clarification of the mechanism of anti-cancer ,indomethacin can become the choice of prevention and treatment of cancers.
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