title: Protective effect of cyclosporin A on brain injury in rats with acute necrotic pancreatitis.
abstract: OBJECTIVE
  This study was designed to evaluate the protective effect of cyclosporin A (CsA) on brain injury in rats with acute necrotic pancreatitis (ANP) in order to provide a scientific basis for the use of the drug in treating brain injury caused by pancreatitis.
  
  
  METHODS
  The rats were divided into a sham group, an ANP group and an ANP+CsA group. The ANP model was induced by administering 5% sodium taurocholate through the biliopancreatic duct. Five minutes before the preparation of the ANP model, 1 ml of CsA (10mg/kg) was injected in a clinically used pharmaceutical formulation (Sandimmun) via the dorsal vein of the penis. Twelve hours after the model was established, samples were taken from the rats in all groups for measurement of appropriate indexes. The serum levels of pro-inflammatory tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta (IL-1beta), and anti-inflammatory interleukin 10 (IL-10) were determined by ELISA. The pancreatic mRNA expressions of these cytokines were evaluated by RT-PCR. Brain water content was tested by the dry-wet method, and brain malondialdehyde (MDA) content was detected by the chemical colorimetry method.
  
  
  RESULTS
  Both the serum levels and the pancreatic tissue mRNA expression of TNF-alpha and IL-1beta, as well as the brain water content and brain MDA content, were significantly increased in the ANP group. CsA treatment noticeably reduced both the serum levels and the pancreatic mRNA expression of TNF-alpha and IL-1beta and decreased brain water and MDA contents. In contrast to the pro-inflammatory cytokines, the serum levels and the pancreatic tissue mRNA expression of IL-10 were markedly increased by the injection of CsA.
  
  
  CONCLUSIONS
  CsA could alleviate acute pancreatitis-associated brain injury.
authors.affiliation: Department of Hepatobiliary Surgery, Xi-Jing Hospital, Fourth Military Medical University, Xi'an, People's Republic of China.
authors.forename: Nian-Song
authors.initials: NS
authors.lastname: Qian
authors.forename: Xiao-Ping
authors.initials: XP
authors.lastname: Xu
authors.forename: Yong
authors.initials: Y
authors.lastname: Chen
authors.forename: Ke-Feng
authors.initials: KF
authors.lastname: Dou
authors.forename: Ya-Yun
authors.initials: YY
authors.lastname: Wang
authors.forename: Yan-Ling
authors.initials: YL
authors.lastname: Yang
mesh_terms: D000818:Animals; D001834:Body Water / Q000378:metabolism; D001930:Brain Injuries / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D016572:Cyclosporine / Q000494:pharmacology*; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D005786:Gene Expression Regulation / Q000187:drug effects*; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D016753:Interleukin-10 / Q000378:metabolism; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D019283:Pancreatitis, Acute Necrotizing / Q000150:complications* / Q000503:physiopathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D007166:Immunosuppressive Agents; D053583:Interleukin-1beta; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D008315:Malondialdehyde; D016572:Cyclosporine