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Objective To study the inhibitory effect of aspirin on proliferation of human hepatocellular carcinoma HepG2 cell line and its possible mechanismt. Methods MTT assay and plate cloning experiments was used to detect proliferation of human hepatoma HepG2 cells. Effects of aspirin on autophagosomes in HepG2 cells were detected by acridine orange fluorescence staining. The expression of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) protein in human hepatocellular carcinoma HepG2 cells was detected by Western blot. Results 10 mmol/L concentration of aspirin could inhibit the proliferation of HepG2 cells, but increase the number of autophagosomes of HepG2 cells, increase AMPK expression, decrease mTOR expression. After combination treatemnt with 40 μmol/L autophagy inhibitor chloroquine (CQ), CQ could enhance the inhibitory effect of 10 mmol/L aspirin on proliferation of human hepatoma HepG2 cells. Conclusion Combination treatment with autophagy inhibitor CQ attenuates 10 mmol/L aspirin-induced autophagy thus enhance its anti-HepG2 effect.
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Objective The objective of this study was to investigate effects of lycopene(LP) on the proliferation and apoptosis of human hepatocellular carcinoma HepG2 cells and to explore its mechanism.Methods HepG2 cells in logarithmic growth phase were treated with 0,5,10,20 μg/mL of LP and 40 μg/mL of Cisplatin for 48 h.Ten replicates in each dose were designed in this study.After treatments,the cell viability was measured by MTT colorimetric assay.The distribution of cell cycle was detected by flow cytometry(FCM).The mRNA expression of Bax and Bcl-2 were measured by RT-PCR.The expression of Caspase-3 protein was explored by Western blot.Results The inhibition rate of HepG2 cells was significantly increased by 10 μg/mL and 20μ g/mL of LP or 40 μg/mL of cisplatin when compared to the negative control group.The cell cycle of HepG2 cells were arrested at the G0/G1 phase and the apoptosis rate were significantly increased in comparison with the negative control group.The level of Bax mRNA expression was significantly increased and decreased in the expression of Bcl-2 mRNA.They were shown an increasing ratio of Bax/Bcl-2 and up-regulated Caspase-3 protein in HepG2 cells treated with LP.All effects in this study show a dose-dependent manner.Conclusion LP can inhibit the proliferation and promote the apoptosis in HepG2 cells.This mechanism may be contributed to arresting cell cycle and regulating gene expression related to apoptosis.
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OBJECTIVE:To study induction effect of entecavir on the apoptosis of hepatocellular carcinoma HepG2 cells and its mechanism. METHODS:After treated with 0(normal control),10,30 and 100 μmol/L(low,medium and high concentration groups)entecavir for 48 h,MTT method was adopted to detect HepG2 cell viability. AnnexinⅤ-PI flow double staining was used to detect cell apoptosis. Western blot was used to determine the phosphorylation of nuclear factor kappa B p65(NF-κB p65)and nu-clear factor kappa B inhibitor α(IκBα),and the protein expression of Bax,Bcl-2,Survivin and C-myc. RESULTS:Compared with normal control group,the cell viability,the phosphorylation of NF-κB p65 and IκBα,and the protein expression of Survivin, C-myc and Bcl-2 of entecavir low,medium and high concentration groups all decreased;the apoptotic rate,the protein expression of Bax increased(P<0.05 or P<0.01),in concentration-dependent manner. CONCLUSIONS:Entecavir can decrease viability of HepG2 cells and induce cell apoptosis,which is related to up-regulation expression of Bax,down-regulation expression of Sur-vivin,C-myc and Bcl-2,and blocking the activation of NF-κB/IκBαsignaling pathway.
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Objective: To investigate the inhibitory effect of Undaria pinnatifida polysaccharides (UPPS) on hepatocellular carcinoma HepG-2 cells and its possible mechanism. Method: The effect of inhibiting proliferation and inducting apoptosis of UPPS were determined by means of MTT and FCM. The expression of Bcl-2 and Bax proteins was immunohis to chemcally evaluated after treatment of UPPS. Results: UPPS inhibited HepG-2 cells growth in vitro , significantly higher than the negative control group (P