Benzaldehyde levofloxacin schiff base induces apoptosis of human hepatocarcinoma cells
10.3969/j.issn.1001-1978.2015.06.017
- VernacularTitle:苯甲醛左氧氟沙星席夫碱诱导人肝癌细胞凋亡作用
- Author:
Fei HUO
;
Naifu TANG
;
Yuanyuan FAN
;
Shimeng LIU
;
Ying ZHANG
;
Hongxia LIANG
;
Guoqiang HU
;
Bin LIU
- Publication Type:Journal Article
- Keywords:
fluoroquinolones schiff base;
hepatocarci-noma cells;
cell proliferation;
apoptosis;
mitochondrial membrane potential;
p53
- From:
Chinese Pharmacological Bulletin
2015;(6):821-826
- CountryChina
- Language:Chinese
-
Abstract:
Aim To study the effect of (S) -1, 8-(2-methyl phosphate ethoxy )-6-fluorine-7-( 4-methyl- pi-perazine-1-base )-3-[ S-benzyls-based-4-( for nitroben-zene methylene group amino )-1 , 2 , 4-all triazole-3 base]-quinoline ( 1-H )-4-ketone ( M18 ) on apoptosis of hepatocarcinoma SMMC-7721 cells in vitro. Meth-ods With different concentrations of M18 at different time used to treat SMMC-7721 cells, human breast cancer MB-231cells, human colon cancer HCT-116 cells, human hepatocarcinoma HEPG-2 cells, mouse bone marrow mesenchymal stem cells ( BMSCs ) in vitro,the inhibition effects of M18 on cell proliferation were examined by MTT assay. Cell apoptosis was de-termined using Hoechst 33258 fluorescence staining and TUNEL method. Mitochondrial membrane poten-tial (△ψm ) was measured using a high content screening image system. Protein expression of caspase-3 , p53 and cytochrome C was detected with Western blot analysis. Results Treatment with M18 ( 4 ~32μmol·L-1 ) potently inhibited the proliferation of the cancer cells in time-and dose-dependent manners ( the IC50 value at 24 h in SMMC-7721 cells, MB-231cells,
HCT-116 cells and HEPG-2 cells was 8. 65 μmol · L-1 , 9. 37 μmol · L-1 , 12. 74 μmol · L-1 and 9. 40μmol · L-1 , respectively ) . In contrast, M18 had weak cytotoxicity against BMSCs with IC50 value of 38. 96 μmol·L-1 . Levofloxacin had weak cytotoxicity against SMMC-7721 cells with IC50 value of 735. 10μmol·L-1 . Treatment of SMMC-7721cells with differ-ent concentrations of M18 for 24 h increased the per-centage of the apoptosis cells ( P <0. 05 ) and de-creased the mitochondrial membrane potential. In ad-dition, M18 increased protein expression of p53, caspase-3 and the cleaved activated forms of caspase-3 in SMMC-7721 cells. Treatment of SMMC-7721 cells with M18 significantly increased cytochrome C in the cytosol, and decreased cytochrome C in the mitochon-drial compartment. Conclusion The mitochondrial-dependent pathways are involved in M18 induction of apoptosis of SMMC-7721 cells.
