title: Pioglitazone: a promising therapeutic tool in sodium taurocholate-induced severe acute pancreatitis.
abstract: BACKGROUND
  Studies suggest that peroxisome proliferator-activated receptor γ(PPARγ) ligands may represent a therapeutic option in acute pancreatitis, yet most of them have been prophylactic administrated.
  
  
  OBJECTIVE
  To evaluate the therapeutic effect of pioglitazone in rats with severe acute pancreatitis induced by sodium taurocholate.
  
  
  METHODS
  Severe acute pancreatitis (SAP) was induced in male Sprague-Dawley rats by the retrograde injection of 5% sodium taurocholate into the pancreatic duct. After SAP was induced, pioglitazone was injected intraperitoneally and its role on the severity of inflammatory response and pancreatic injury was investigated. Amylase activity, inflammatory cytokines production, pathological changes of pancreas, PPARγ mRNA expression, and the survival rate were examined.
  
  
  RESULTS
  Treatment with pioglitazone decreased the level of amylase activity, proinflammatory factors IL-6 and TNF-α, ameliorated pancreatic histological score, and upregulated the expression of PPARγ mRNA. The survival rate in the early stage of severe acute pancreatitis was also improved.
  
  
  CONCLUSIONS
  Pioglitazone can be used as a therapeutic drug and relieve the damages caused by SAP, which suggests PPARγ ligand-pioglitazone offers a potent approach for the treatment of severe acute pancreatitis.
authors.affiliation: Department of Gastroenterology, Branch Hospital of the First People's Hospital, Shanghai Jiao Tong University, School of Medicine, 201600, Shanghai, China. yfyxp@yahoo.com.cn
authors.forename: Ping
authors.initials: P
authors.lastname: Xu
authors.forename: Kai
authors.initials: K
authors.lastname: Xu
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.forename: Jin-Ping
authors.initials: JP
authors.lastname: Jiang
authors.forename: Ling-Quan
authors.initials: LQ
authors.lastname: Chen
mesh_terms: D000681:Amylases / Q000096:biosynthesis; D000818:Animals; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D015850:Interleukin-6 / Q000096:biosynthesis; D008297:Male; D047495:PPAR gamma / Q000819:agonists; D010179:Pancreas / Q000187:drug effects / Q000473:pathology; D019283:Pancreatitis, Acute Necrotizing / Q000139:chemically induced / Q000188:drug therapy* / Q000401:mortality / Q000473:pathology; D000077205:Pioglitazone; D051381:Rats; D017207:Rats, Sprague-Dawley; D012720:Severity of Illness Index; D013656:Taurocholic Acid / Q000009:adverse effects; D045162:Thiazolidinediones / Q000627:therapeutic use*; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D007004:Hypoglycemic Agents; D015850:Interleukin-6; D047495:PPAR gamma; D045162:Thiazolidinediones; D014409:Tumor Necrosis Factor-alpha; D013656:Taurocholic Acid; D000681:Amylases; D000077205:Pioglitazone
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