p-Methoxycinnamaldehyde levofloxacin-3-ylhydrazone induces apoptosis of human hepatocarcinoma SMMC-7721 cells

Aim To study the effect of(S) N-(3-p-methoxylphenyl)-6-fluoro-7-(4-methylpiperazin-1-yl)-1,8-(3,1-propoxy)-quinolin-4(1H)-one-3-carbonyl hydrazine(FQ-10) on apoptosis of hepatocarcinoma SMMC-7721 cells in vitro.Methods With different concentrations of FQ-10 at different times used to treat SMMC-7721 cells in vitro,the proliferation of the cells and the inhibition effect of FQ-10 on the cell proliferation were examined by MTT assay.Cell apoptosis was determined by Hoechst 33258/PI fluorescence staining,TUNEL and agarose gel electrophoresis method.Mitochondrial membrane potential(MMP,△ψm) was measured by high content screening image system.The caspase-9,caspase-8,caspase-3,p53,Bcl-2 and Bax protein expressions were detected by Western blot analysis.Results The cell proliferation was inhibited by FQ-10 at 0.625~10.00 μmol·L-1 in a time-and-dose dependent manner.Treatment of SMMC-7721 cells with different concentrations of FQ-Henan 10 for 24 h increased the percentage of the apoptosis cells(P0.05).The typical ladder DNA in apoptotic cells and a concomitant dissipation of the mitochondrial membrane potential could be observed by agarose gel electrophoresis.Typical cell apoptotic features could be seen and specific PI staining was observed in late apoptotic cells.In addition,FQ-10(3.0~7.39 μmol·L-1) increased protein expression of p53,Bax,caspase-9,caspase-3,separately,and induced cytosolic accumulation of activities caspase-9 and caspase-3,whereas protein expression of Bcl-2 decreased with no change of caspase-8.Conclusion The mitochondrial-dependent pathways were involved in FQ-10 induction of apoptosis of SMMC-7721 cells.