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Effect of sulforaphane combined with sorafenib on the growth inhibition and apoptosis of hepatocellular carcinoma HepG2 cells
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DOI   10.11656/j.issn.1672-1519.2019.12.20
Key Words   sulforaphane;sorafenib;hepatocellular carcinoma cells;synergistic effect
Author NameAffiliationE-mail
HUANG Jianfeng Department of Hepato-Pancreato-Biliary Surgery, Affiliated Hospital of Hubei University for Nationalities, Enshi 445000, China  
WEI Xiaodong Department of Cardiothoracic Surgery, Affiliated Hospital of Hubei University for Nationalities, Enshi 445000, China  
ZHAI Dongsheng Department of Hepato-Pancreato-Biliary Surgery, Affiliated Hospital of Hubei University for Nationalities, Enshi 445000, China 203265147@qq.com 
Abstract
    [Objective] To observe the effects of sulforaphane combined with sorafenib on the hepatocellular carcinoma HepG2 cells and study its mechanism.[Methods] The anti-proliferation effects of either sulforaphane or sorafenib alone or their combination on HepG2 cells were assessed by CCK8 assay. The IC50 values of two single drug and the CI values were calculated. The apoptosis ratios were analyzed by flow cytometer. The expression of ClinD1,C-myc,Bcl-2,Bax,p-NF-κB and p-IκB α were detected by Western blotting.[Results] The anti-proliferation and apoptosis induction effects were more remarkably than the two single drugs when combination with sulforaphane and sorafenib (P<0.05). It appeared in a concentration-dependent manner. The CI values of sulforaphane combinated with sorafenib were all less than alone,which had a synergistic effect. Western blotting showed that sulforaphane combinated with sorafenib could significantly decrease the expression levels of ClinD1,C-myc,Bcl-2,p-NF-κB and p-IκBα and increase the expression level of Bax in HepG2 cells,as compared with the control and the single drugs (P<0.05).[Conclusion] The combination of sulforaphane and sorafenib performs a synergistic anti-tumor effect on HepG2 cells,and its mechanism underlying may be related to apoptosis and down-regulation the activation of NF-κB pathway.

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