Objective To investigate the effect of maslinic acid(MA)on the proliferation and apoptosis of mouse colon cancer CT26 cells through IL-6/STAT3 signaling pathway.Methods CT26 cells were cultured in vitro,then treated with 0,10,20,30,35,and 40 μmoL·L-1 MA.After 24 hours of intervention,the effect MA on cell viability was detected by CCK-8 method,the expression of IL-6 mRNA was detected by RT-PCR,the apoptosis rate was detected by flow cytometry,and the expression levels of STAT3 pathway-related proteins in each group were detected by Western blotting.Control group,IL-6(20 ng·µL-1)stimulation group and costimulation groups with different concentrations of MA and IL-6 were set up,and the ex-pression levels of p-STAT3 and STAT3 protein in each group were detected by Western blotting.The expression levels of p-STAT3 and STAT3 protein in cells treated with MA,a phosphatase inhibitor(sodium orthovanadate),or MA+Sodium Or-thovanadate simultaneously were detected by Western blotting.Results CCK-8 results showed that MA decreased the viability of CT26 cells compared with control group(P＜0.05),IC50=37.32 μmoL·L-1.RT-PCR results showed that IL-6 mR-NA expression levels in 30,35,40 μmoL·L-1 administration groups were decreased(P＜0.05).Flow cytometry analysis showed that the apoptosis rate was increased in 30,35 and 40 μmoL·L-1 administration groups(P＜0.05).Western blotting results showed that the expression levels of p-STAT3 and Bcl-2 protein in 35 and 40 µmoL·L-1 administration groups were decreased(P＜0.05).Sodium Orthovanadate can restore the p-STAT3 protein level that was reduced in the MA alone group(P＜0.05).Conclusion MA may reduce the expression level of IL-6 and further inhibit the phosphorylation of STAT3,thereby reducing the expression of anti-apoptotic protein Bcl-2,promoting tumor cells apoptosis and inhibiting their proliferation.
维普
万方数据