title: Inflexinol reduces severity of acute pancreatitis by inhibiting nuclear factor-κB activation in cerulein-induced pancreatitis.
abstract: OBJECTIVE
  To examine the effect of inflexinol on the development of acute pancreatitis (AP) and to investigate the mechanisms responsible for the protective effect against AP.
  
  
  METHODS
  Acute pancreatitis was induced in mice by intraperitoneal injection of cerulein. Inflexinol was administered intraperitoneally 4 times every 6 hours from 1 hour before the first cerulein injection. Serum amylase activity and histology of the pancreas were measured. Determination of pancreatic nuclear factor-κB (NF-κB) p65 expression was conducted by Western blotting and immunohistochemistry to investigate the mechanisms responsible for the inflexinol effects.
  
  
  RESULTS
  Serum amylase activity in the cerulein group was significantly higher than that in the control group (P < 0.05). Pancreatic histology revealed marked inflammatory changes in the cerulein group such as interstitial edema, vacuolization, necrosis, and infiltration of inflammatory cells; and Western blotting and immunohistochemistry showed marked NF-κB p65 expression. Treatment with inflexinol significantly attenuated the inflammatory changes in pancreatic histology at 24, 48, and 72 hours (P < 0.05). Pancreatic NF-κB p65 expression decreased significantly after inflexinol treatment (P < 0.05).
  
  
  CONCLUSIONS
  Inflexinol reduced the severity of cerulein-induced AP by inhibiting NF-κB activation.
authors.affiliation: Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul, Korea.
authors.forename: Dong-Won
authors.initials: DW
authors.lastname: Ahn
authors.forename: Ji Kon
authors.initials: JK
authors.lastname: Ryu
authors.forename: Jaihwan
authors.initials: J
authors.lastname: Kim
authors.forename: Yong-Tae
authors.initials: YT
authors.lastname: Kim
authors.forename: Yong Bum
authors.initials: YB
authors.lastname: Yoon
authors.forename: Kyoungbun
authors.initials: K
authors.lastname: Lee
authors.forename: Jin Tae
authors.initials: JT
authors.lastname: Hong
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D015415:Biomarkers / Q000097:blood; D015153:Blotting, Western; D002108:Ceruletide; D004195:Disease Models, Animal; D045786:Diterpenes, Kaurane / Q000494:pharmacology*; D005260:Female; D007150:Immunohistochemistry; D051379:Mice; D008807:Mice, Inbred BALB C; D010179:Pancreas / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D010195:Pancreatitis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D012720:Severity of Illness Index; D013997:Time Factors; D051996:Transcription Factor RelA / Q000378:metabolism*
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D045786:Diterpenes, Kaurane; C498144:Rela protein, mouse; D051996:Transcription Factor RelA; C530049:ent-1,3,6,11-tetrahydroxykaur-16-ene-15-one 3,11-diacetate; D002108:Ceruletide; D000681:Amylases