title: [CHL prevent colon neoplasms in mice and its selective inhibition on COX-2].
abstract: OBJECTIVE
  Chlorophyllin (CHL) was proved to have strong anti-inducement effect toward many mutagens and epicarcinogens. This study was to explore effect of CHL in preventing colon neoplasms in mice induced by dimethylhydrazine (DMH), and the selective inhibition on cyclooxygenase 2(COX-2).
  
  
  METHODS
  The colorectal neoplasms were induced with DMH in mice and the different dose of CHL were administered in different phases, then the prevention of colorectal neoplasms by CHL was examined; The IC50 and growth curve of HT29 cells were measured with MTT method after treated with CHL; The effect of CHL on the expression of COX-1 mRNA and COX-2 mRNA in HT29 cells were measured with RT-PCR method; The effect of CHL on the expression of COX-2 protein and NF-kappaB protein were measured with western blot and immunohistochemistry methods.
  
  
  RESULTS
  The incidence of colon cancer, average tumor amount, and percentage of carcinoma in CHL group were significantly lower than those in DMH group (P< .05); CHL could inhibit the growth of HT29 cells. The effects were dose dependent; CHL could selectively inhibit the expression of COX-2mRNA in HT29 cells,the expression of COX-2 protein in colon neoplasms and HT29 cells, and the expression of NF-kappaB protein in colon neoplasms.
  
  
  CONCLUSIONS
  CHL could prevent colon neoplasms in mice induced by DMH and the preventive effect related to selective inhibition on COX-2, furthermore, the inhibition of CHL on COX-2 was realized by inhibiting NF-kappaB protein.
authors.affiliation: Department of Surgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang, 310022, P.R.China. dingxwyh@163.com
authors.forename: Xiao-Wen
authors.initials: XW
authors.lastname: Ding
authors.forename: Xiao-Li
authors.initials: XL
authors.lastname: Ding
authors.forename: Shu
authors.initials: S
authors.lastname: Zheng
authors.forename: Hong-Jian
authors.initials: HJ
authors.lastname: Yang
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002735:Chlorophyllides / Q000494:pharmacology* / Q000627:therapeutic use; D003106:Colon / Q000378:metabolism; D015179:Colorectal Neoplasms / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D004127:Dimethylhydrazines; D019073:HT29 Cells / Q000378:metabolism; D006801:Humans; D008297:Male; D008565:Membrane Proteins; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism; D011451:Prostaglandin-Endoperoxide Synthases / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011897:Random Allocation
chemical_list: D016588:Anticarcinogenic Agents; D002735:Chlorophyllides; D004127:Dimethylhydrazines; D008565:Membrane Proteins; D016328:NF-kappa B; D012333:RNA, Messenger; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C496511:PTGS1 protein, human; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; C496512:Ptgs1 protein, mouse; C007020:chlorophyllin