Effects of dihydroartemisinin on prostate cancer growth in vivo and expression of Casnase-3
AIM: To study the inhibitory effects of dihydroartemisinin on the growth of transplantation human prostate cancer PC-3 cells in nude mice and on the expression level of Caspase-3 and to explore the underlying action mechanism. METHODS: Prostate cancer PC-3 cells were transplanted into 20 nude mice to establish the solid tumor mode. These nude mice were randomly divided into 4 groups, with 5 mice in each group: Control group, solvent group, low dose dihydroartemisinin group and large dose dihydroartemisinin group. The tumor growth inhibition rates were calculated on day 13 after drug administration. Pathomorphism changes of PC-3 cells were observed by light microscope and transmission electron microscope after administration. The cells were stained with Hoechst 33258 and examined under fluorescence microscope to determine cell apoptosis. The positive products of Caspase-3 were tested by immunohistochemical method. RESULTS: The tumor weight of dihydroartemisinin groups were obviously smaller than that of both control group and solvent group (P < 0. 05 ). The tumor growth inhibition rates in large dose dihydroartemisinin group and low dose dihydroartemisinin group were 69.221% and 63.186%. Light microscope and transmission electron microscope examination revealed that the scattered apoptotic cells and bodies were observed in tumor tissues in dihydroartemisinin groups. Fluorescence microscope examination revealed that the apoptotic cells stained by Hoechst 33258 significantly increased in tumor tissues in dihydroartemisinin groups. The number density of apoptotic cell significantly augmented (P < 0.05 ). Immunohistochemical examination revealed that the positive products of Caspase-3 significantly increased in dihydroartemisinin groups(P<0.05). CONCLUSION: These results demonstrated that dihydroartemisinin has strong inhibitory effects on human prostate cancer cell line PC-3 cells in vivo. The action mechanism might be related with the upregulation of Caspase-3.
NETL
NSTL
万方数据
维普
