RESUMO
Objective To investigate the possible molecular mechanism for alpha(α)-mangostin's inhibition of the proliferation and apoptosis of human gastric cancer cells.Methods Human gastric adenocarcinoma SGC7901 cell line was treated with α-mangostin.CCK8 method was used to measure the viability of SGC7901 cells.The effect of α-mangostin on apoptosis and cell cycle was determined by immune fluorescence and flow cytometry.The expression of the relevant proteins was detected using Western blot.The shapiro-wilk test was performed for evaluation of deviation from normality.Normally distributed data was analyzed with one-way ANOVA.Welch test was used in data with heterogeneity of variance and multiple compared by Games-Howell test after that.Results CCK8 results showed that cell viability differed significantly among groups treated with different concentrations of α-mangostin(10,15,20,25,and 30 μmol/L)(P＜0.05).QPCR data showed that the concentration of α-mangostin was positively correlated with mRNA level of LC 3 but not caspase protein(r=0.976,P＜0.05).In 15 μmol/L but not 10 μmol/L α-mangostin treatment system,the autophagy inhibitors 3-MA(10 μmol/L),bafilomycin A(10 μmol/L)and LY294002(10 μmol/L)could significantly alleviate α-mangostin's killing effect on SGC7901 cells(P＜0.05).Conclusion The anti-tumor effects of α-mangostin against human gastric adenocarcinoma cells in vitro can be partly attributed to apoptosis,autophagy and arresting cell phase.