Related Study On The Effect Of Apigenin Combined With Radiotherapy On Promoting Apoptosis Of Human Colon Cancer HCT116 Cells

ObjectivesTo investigate whether apigenin combined with radiotherapy can promote apoptosis of human colon cancer HCT116 cells,and to explore the possible mechanism of apigenin combined with radiotherapy on apoptosis of human colon cancer HCT116 cells.Methods1.The effects of different doses of radiation(0、2、4、6、8 Gy)alone treated human colon cancer HCT116 cells,different concentrations of apigenin(0、10、20μmol / L)alone to treat human colon cancer HCT116 cells,apigenin(20μmol/L)combined with radiation(8Gy)treatment ofhuman colon cancer HCT116 cells on the expression of Bcl-2、caspase-3、Cleaved-PARP-1、AMPK、 p-AMPK(Thr172)、 P53 and p-P53(Ser15).2.The effects of different doses of radiation(0、 2、 4、 6、8 Gy)alone acted on human colon cancer HCT116 cells,and differentconcentrations of apigenin(0、10、 20、30、40、50、60 μmol/L)alonetreated human colon cancer HCT116 cells,and apigenin(20μmol/L)combined with radiation(8 Gy)treated human colon cancer HCT116 cells on intracellular ROS.3.After pretreatment with NAC,the effect of apigenin(20μmol/L)combined with radiation(8Gy)on ROS production in human HCT116 cells,as well as on cells caspase-3,Cleaved-PARP-1,Bcl-2 protein and effects of AMPK、p-AMPK(Thr172)、P53、and p-P53(Ser15)expression.Results1.Compared with the control group,the expression of caspase-3、Cleaved-PARP-1、AMPK、p-AMPK(Thr172)、 p-P53(Ser15)in human colon cancer HCT116 cells treated with radiation alone,apigenin alone and apigenin combined with radiotherapy increased significantly,especially in the combination of Apigenin and radiotherapy.Radiation alone,apigenin alone and apigenin combined with radiotherapy could reduce the expression of Bcl-2 in human colon cancer HCT116 cells,especially in apigenin combined with radiotherapy.The expression of P53 did not change significantly under various treatment factors.2.When irradiated cells were irradiated alone,compared with the control group(0Gy group),radiation could significantly increased the production of ROS in human colon cancer HCT116 cells(P<0.05),andincreased with the increase of radiation dose.When apigenin was treated with cells alone,10 to 60 umol/L of apigenin significantly increased ROS production in human colon cancer HCT116 cells compared with the control group(apigenin 0μmol/L)(P<0.05),and was concentrationdependent.The way to increase.The apigenin(20μmol/L)combined withradiation(8Gy)group significantly increased the production of ROS in human colon cancer HCT116 cells compared with the apigenin(20μmol/L)alone group and the radiation(8Gy)alone group(P<0.01).3.Compared with the treatment group apigenin(20μmol/L)combined radiation(8Gy)group,NAC pretreatment group can significantly reduce the production of ROS in human colon cancer HCT116 cells(P<0.01);after adding NAC pretreatment it can significantly reverse the expression of AMPK,p-AMPK(Thr172),p-P53(Ser15),caspase-3,and Cleaved-PARP-1 proteins induced by apigenin(20μmol/L)combined with radiation(8Gy)group.It can increase theexpression of Bcl-2 protein.Conclusions1.The results showed that apigenin combined with radiotherapy was able to promote the apoptosis of human colon cancer HCT116 cells.2.Apigenin combined with radiotherapy can promote ROS production in human HCT116 cells,and then activate AMPK.After AMPKphosphorylation activation,P53 can be phosphorylated,which can increase the expression of caspase-3,Cleaved-PARP-1 protein and decrease the expression of Bcl-2 and promote cell apoptosis.