Effect Of Acteoside On Proliferation And Apoptosis Of Hepatoma Cells Via P38MAPK Signaling Pathway

Objective: To explore the specific mechanism of acteoside(ACT)affecting the proliferation and apoptosis of hepatoma cells through p38 MAPK signaling pathway,and establish a theoretical basis for the development of anti-HCC drugs with ACT as an active ingredient from the cell and protein levels.Methods: Hep G2 liver cancer cells were used as experimental cells.Flow cytometry was combined with CCK-8 method to determine the optimal concentration(ARHBC)and time of ACT inhibition of hepatoma cell proliferation.The cultured Hep G2 liver cancer cells were divided into a blank control group(Ordinary complete medium),ARHBC group,SB 203580(p38 MAPK inhibitor)+ ARHBC group and SB 203580 group.The effect of ACT on the proliferation of hepatoma cells was detected by CCK-8 method.Western blot was used to detect the expression of p38 MAPK,P-p38 MAPK,p53 and caspase3 proteins.Apoptosis of Hep G2 liver cancer cells was detected by flow cytometry.Results: With the increase of ACT concentration,Hep G2 liver cancer cells are less adherent and tightly arranged.The Hep G2 liver cancer cells with ACT are shortened and rounded compared with normal Hep G2 liver cancer cells,the morphology is gradually full,vacuoles appear in the cells,and floating dead cells appear in the cell culture flask.As the concentration of ACT increases and the prolongation of the action time,the survival rate of Hep G2 liver cancer cells decreased.The optimal inhibitory concentration of ACT was 80 mg /L and the optimal time was 48 h.The ARHBC group had the lowest cell survival rate and the highest apoptotic rate in the four groups of Hep G2 hepatoma cells,and there were significant differences compared with the blank control group(P <0.05).There was no difference in the expression of p38 MAPK in Hep G2 hepatoma cells,but the expression of P-p38 MAPK,p53 and caspase3 in ARHBC group was significantly higher than that in the control group(P <0.05).Conclusion: ACT can inhibits the proliferation and promotes apoptosis of Hep G2 cell through the p38 MAPK signaling pathway.