title: Anti-inflammatory effects of Pulvis Fellis Suis extract in mice with ulcerative colitis.
abstract: BACKGROUND
  Pulvis Fellis Suis is used in folk medicines to treat intestinal diseases, acute pharyngitis, whooping cough and asthma in China. Although several reports indicate that Pulvis Fellis Suis display diverse biological activities, such as antibacterial, anti-inflammatory and anti-infusorian effects, its effects on ulcerative colitis have not been previously explored.
  
  
  OBJECTIVE
  The purpose of the present study is to assess the anti-inflammatory effect of Pulvis Fellis Suis (PFS) extract in acute ulcerative colitis model induced by trinitrobenzene sulfonic acid (TNBS) in mice.
  
  
  METHODS
  Different doses of Pulvis Fellis Suis extract (100, 200 and 400mg/kg/day) and sulfasalazine (500mg/kg/day) were administered by gavage for 7days after the induction of colitis with TNBS. The efficacy of PFS was studied by macroscopical and histological scoring systems as well as myeloperoxidase (MPO) activity. Serum levels, including tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were assayed by enzyme-linked immunoassay. The expression of cyclooxygenase (COX)-2 in the colons was assessed by immunohistochemical analysis.
  
  
  RESULTS
  Treatment with PFS significantly attenuated macroscopic damage as compared with TNBS (P<0.01). Histological analysis showed that PFS improved the microscopic structure and preserved some areas of the colonic mucosa structure. In addition, administration of PFS effectively inhibited COX-2 protein expression and MPO activity accumulation. TNF-α and IL-6 levels were also diminished dose-dependently (P<0.05, P<0.01), and IL-6 level obtained had no significant results by small dose of PFS. All the effects of these parameters were comparable to that of the standard sulfasalazine, especially at the highest dose level.
  
  
  CONCLUSIONS
  We have shown for the first time that PFS has an anti-inflammatory effect in TNBS-induced ulcerative colitis which might be related to the reduction of up-regulated TNF-α and IL-6 production, and that it may have therapeutic value in the setting of inflammatory bowel disease (IBD).
authors.affiliation: Biomedicine Key Laboratory of Shaanxi Province, Northwest University, No. 229 Taibai North Road, Xi'an 710069, People's Republic of China.
authors.forename: Jiao
authors.initials: J
authors.lastname: He
authors.forename: Jinru
authors.initials: J
authors.lastname: Liang
authors.forename: Sha
authors.initials: S
authors.lastname: Zhu
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.forename: Yongmin
authors.initials: Y
authors.lastname: Zhang
authors.forename: Wenji
authors.initials: W
authors.lastname: Sun
mesh_terms: D000208:Acute Disease; D000818:Animals; D001646:Bile; D001688:Biological Products / Q000494:pharmacology / Q000627:therapeutic use*; D003093:Colitis, Ulcerative / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D003106:Colon / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D004305:Dose-Response Relationship, Drug; D015850:Interleukin-6 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009195:Peroxidase / Q000378:metabolism; D012460:Sulfasalazine / Q000494:pharmacology; D034421:Sus scrofa; D014302:Trinitrobenzenesulfonic Acid; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D001688:Biological Products; D052246:Cyclooxygenase 2 Inhibitors; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D012460:Sulfasalazine; D014302:Trinitrobenzenesulfonic Acid; D009195:Peroxidase