Study on molecular mechanism of selenium compounds based on target TrxR in inhibiting the growth of brain gliomas
Objective To explore the molecular mechanism of three organic selenium compounds selenocysteine(SeC),metholenic acid(MeSe)and selenomethionine(SeMe)based on thioredoxin reductase(TrxR)target in inhibiting the growth of brain gliomas.Methods Human glioblastoma cells and para-cancerous tissue cells in U251 and U87 were studied.Human glioblastoma cells were included in the observation group and para-cancerous tissue cells in the control group.The cells were treated with different concentrations of selenium compounds for a certain period of time.Western blot assay was used to detect the changes of TrxR protein expression;DCF-flow cytometry was used to observe the changes of cellular oxidative stress reactive oxygen species(ROS)in the cells treated with selenium compounds;TdT-mediated dUTP nick-end labeling(TUNEL)technique was used to label the broken DNA and observe the apoptosis of cells.The expression levels of TrxR protein were compared between the two groups,and the effects of SeC,MeSe and SeMe on cell activity,expression level of TrxR protein and ROS expression level in cells of the observation group were analyzed.Results The TrxR protein expression levels of U251 and U87 human malignant glioma cells in the observation group were(26.92±2.14)and(26.76±2.32)ng/ml,which were higher than(1.09±0.21)ng/ml in the control group,with statistical significance(P<0.001).The activity of U251 and U87 human malignant glioma cells gradually decreased with the increase of SeC,MeSe,and SeMe concentrations.Compared with pre-intervention,after SeC,MeSe,and SeMe intervention,TrxR protein expression decreased in U251 and U87 human malignant glioma cell tissues,with statistical significance(P<0.001).Compared with pre-intervention,after SeC,MeSe,and SeMe interventions,ROS expression levels increased in U251 and U87 human malignant glioma cell tissues,with statistical significance(P<0.001).Conclusion Selenium compounds inhibit the growth of glioma by increasing ROS expression based on TrxR.