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WANG Zhang-gui, SUN Guo-ping, XU Shu-ping, WANG Hua, LIU Si-han. Anti-proliferative Effect of Combining Paeonol and Doxorubicin on HepG2 Cell[J]. Cancer Research on Prevention and Treatment, 2008, 35(06): 386-389. DOI: 10.3971/j.issn.1000-8578.2338
Citation: WANG Zhang-gui, SUN Guo-ping, XU Shu-ping, WANG Hua, LIU Si-han. Anti-proliferative Effect of Combining Paeonol and Doxorubicin on HepG2 Cell[J]. Cancer Research on Prevention and Treatment, 2008, 35(06): 386-389. DOI: 10.3971/j.issn.1000-8578.2338

Anti-proliferative Effect of Combining Paeonol and Doxorubicin on HepG2 Cell

  • Objective  To explore the anti2proliferative effect of combining Paeonol and Doxorubicin on Hep G2 cell and possible mechanism. Methods  The inhibitor effect of Paeonol or Doxorubicin alone or in both on Hep G2 cell was measured by MTT assay. The coefficient of drug interaction was used to analyze the nature of drug interactions. The apoptosis rate was detected by flow cytomet ry and the morphological change of apopotosis was observed by TUNEL. Bcl22 and Bax expression were assayed by Western blot . Results  Pae or Dox had anti2proliferative effect on Hep G2 cell in a dose2dependent manner. The coeffi2 cient of drug interaction ( CDI < 0. 7) was significant af ter t reatment with a combination of Pae (31. 25 mg/ L) with Dox (0. 16 、0. 31 mg/ L) . The cells showed distinctive apoptotic characteristics by TUNEL and the apoptosis rate of the combined group (37. 0 %) was higher than those of the group t reated with Pae (6. 49 %) or Dox (5. 41 %) alone at the desired concent rations by flow cytomet ry assay. The expres2 sion of Bcl22 decreased and that of Bax increased in the t reated groups, especially in the combination group . The ratio of Bcl22/ Bax decreased conspicuously. Conclusion  Pae could enhance the anti2prolifera2 tive effect of Dox on Hep G2 cell at designated concent rations and the possibility mechanism may be in2 duce apoptosis via activation of Bax and down2regulation Bcl22, which may be useful in hepatocarcinoma t reatment .
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