Study On The Effect And Molecular Mechanism Of Celastrol Anti-gastric Cancer Cells

ObjectiveTo investigate the effects of Celastrol on the proliferation,migration and apoptosis of human gastric cancer cells(SGC-7901,HGC-27),and to explore its related mechanism,we will provide laboratory data for the clinical research of gastric cancer.Methods1.MTT assay was used to detect the effect of celastrol on the proliferation of human gastric cancer cells.0,0.5,1.0,1.5,2.0,3.0,4.0 ?M celastrol was acted to SGC-7901 cells and HGC-27 cells for detecting the effect on the proliferation of human gastric cancer cells.2,Cells scratch repair experiment was used to detect the effect of celastrol on the migration of human gastric cancer cells.0,1.0,2.0,3.0 ?M celastrol was acted to SGC-7901 cells,and 0,0.5,1.0,1.5 ?M celastrol was acted to HGC-27 cells to analyze the migration of human gastric cancer cells.3.Flow cytometry was used to detect cell cycle and apoptosis rate.The effects of 0,0.5,1.0,1.5 ?M celastrol on HGC-27 cells were observed and their effects on cell apoptosis and cell cycle were observed.4.The effect of celastrol on the expression of apoptosis-related proteins in HGC-27 cells was detected by Western blot.Results1.The effect of celastrol on the morphology of gastric cancer cells.Microscopic observation showed that by increased of the concentration of tripterine and the prolongation of the action time,the absolute numbers of cells decreased,the cell size reduction and shrink and cell became round.Some cells no longer adhered also floated up with the nucleus shrank compared with the control group.2.The results of MTT assay showed that celastrol inhibited the proliferation of human gastric cancer cells HGC-27 and SGC-7901 in a dose-and time-dependent manner(P<0.01).3.Cells scratch repair experiment showed that celastrol significantly inhibited the migration of human gastric cancer cells HGC-27 and SGC-7901 in a dose-and time-dependent manner compared with the control group(P<0.01).4.The results of flow cytometry detection of apoptotic rate showed that celastrol significantly increased the early apoptotic rate of human gastric cancer cell HGC-27 in a concentration-dependent manner,comparing with the control group(P<0.01).5.The results of flow cytometry detection of cell cycle showed that celastrol increased the G1 phase and decreased the S phase of human gastric cancer cells,which was concentration-dependent comparing with the control group(P<0.01).6.Compared with the control group,western blot data showed that,celastrol increased,the expression of Bax,Cleaved Caspase-3,p-p38,and decreased the expression of Bcl-2 and p-ERK.in human gastric cancer cells(HGC-27)(P<0.01).ConclusionCelastrol inhibits the proliferation and migration of human gastric cancer cells and induces apoptosis to exert its anti-cancer effect.The mechanism may be related to up-regulation of Bax,Cleaved Caspase-3,p-p38,and down-regulation of Bcl-2 and p-ERK.