| Lycorine is a kind of natural alkaloid extracted from Alaryllidaceae that has shown various pharmacological effects,such as anti-tumor,anti-bacterial,anti-viral,and the effects on the central nervous system and cardiovascular system In recent years,though domestic and foreign experts to work on a lot of lycorine research,some pharnacological effects and mechanism is not very clear.So this experiment studied on mechanism apoptosis of HepG-2 cells induced by lycorine through death receptor pathway,provides a theoretical basis for the anti-tumor mechanism of lycorine.In this study,Western Blotting analysis was used to show the expression of protein Fas and FasL when HepG-2 cells was induced by lycorine at the dose of 3μmol/L、6μmol/L、12μmol/L after 48h.The flow cytometry detected the expression of protein TRAIL and DR5 at the different concentrations of lycorine,when HepG-2 cells was induced by lycorine after 48h.The microplate reader was used to detect the activity of protein Caspase-3,Caspase-8 in HepG-2 cells when the dose of 3μmol/L、6μmol/L、12μmol/L of lycorine acted on the cells after 48h by Caspase-3 and Caspase-8 kit.The results showed that the relative protein expression were Fas:103.26%、108.45%、118.60%,FasL:106.38%、132.32%、148.04%,lycorine can increase the expression of protein Fas and FasL significantly,and as the dose increased,the protein expression was gradually increasing(P<0.01).The flow cytometry showed that the relative protein expression were DR5:64.60%、79.33%、91.83%,TRAIL:75.47%、95.90%、96.77%,and as the dose increased,the protein expression was gradually increasing(P<0.01).The results showed that lycorine can promote the activity of protein Caspase-3,Caspase-8 in HepG-2 cells,the expression of protein Caspase-3:137.22%、163.38%、207.62%,Caspase-8:153.45%、163.92%、243.65%,as the dose increased,the protein expression was gradually increasing(P<0.01).These results indicated that lycorine upregulated the expression of protein Fas/FasL and DR5/TRAIL,enhanced the activity of protein Caspase-8 and Caspase-3 in HepG-2 cells,and induced the apoptosis of HepG-2 cells through death receptor pathway. |