title: [Inhibitory effects of celecoxib combined with capecitabine on H22 hepatoma mice and its mechanism].
abstract: OBJECTIVE
  To evaluate the inhibitory effect and its mechanism of celecoxib combined with capecitabine on the growth of implanted H22 hepatoma in mice.
  
  
  METHODS
  Tumor model was established by hypodermical injection of H22 cells in BALB/c nude mice. Forty mice were equally randomly divided into 4 groups: control group, celecoxib group (receiving 100 mg/kg celecoxib), capecitabine group (receiving 755 mg/kg capecitabine), and combined treatment group (receiving 100 mg/kg of celecoxib and 755 mg/kg of capecitabine). From the third post-implantation day, each mouse was given relevant drug (or normal saline) by oral gavage. Fifteen days later, all mice were sacrificed and the tumor tissues were measured. The mRNA and protein levels of nuclear factor kappa-B (NF-ΚB) p65 and cyclooxygenase (COX)-2 in tumor tissues were detected by the quantitative polymerase chain reaction (qPCR)and Western blotting, respectively.
  
  
  RESULTS
  The tumor inhibition rate was 30.2% in celecoxib group and 49.9% in capecitabine group, which was significantly lower than that (75.4%) in the combined treatment group (P<0.01,P<0.05, respectively). qPCR showed a significant decrease of the mRNA expression of COX-2 in celecoxib group and combined treatment group when compared with control group (P<0.001), but no significant change in NF-ΚB p65.Capecitabine had no significant effects on the mRNA expression of COX-2 and NF-ΚB p65. Western blotting showed that celecoxib and combined treatment significantly inhibited the protein expression of COX-2 and NF-ΚB p65(P<0.05), but not capecitabine.
  
  
  CONCLUSIONS
  Celecoxib can enhance the antitumor effect of capecitabine by inhibiting the expressions of COX-2 and NF-ΚB p65 in mice bearing H22 implanted tumor.
authors.affiliation: Department of Medical Oncology, Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou,China.
authors.forename: Zhi-hua
authors.initials: ZH
authors.lastname: Yao
authors.forename: Ya-dong
authors.initials: YD
authors.lastname: Yuan
authors.forename: Yan-yan
authors.initials: YY
authors.lastname: Liu
authors.forename: Hong-qiang
authors.initials: HQ
authors.lastname: Guo
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhao
authors.forename: Shu-na
authors.initials: SN
authors.lastname: Yao
authors.forename: Shu-jun
authors.initials: SJ
authors.lastname: Yang
mesh_terms: D000818:Animals; D000069287:Capecitabine; D000068579:Celecoxib; D045744:Cell Line, Tumor; D051546:Cyclooxygenase 2 / Q000378:metabolism; D003841:Deoxycytidine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D004357:Drug Synergism; D005472:Fluorouracil / Q000031:analogs & derivatives* / Q000627:therapeutic use; D008113:Liver Neoplasms / Q000188:drug therapy*; D051379:Mice; D008807:Mice, Inbred BALB C; D009368:Neoplasm Transplantation; D011720:Pyrazoles / Q000627:therapeutic use*; D013449:Sulfonamides / Q000627:therapeutic use*; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: D011720:Pyrazoles; C498144:Rela protein, mouse; D013449:Sulfonamides; D051996:Transcription Factor RelA; D003841:Deoxycytidine; D000069287:Capecitabine; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D000068579:Celecoxib; D005472:Fluorouracil