title: Thymosin alpha 1 improves severe acute pancreatitis in rats via regulation of peripheral T cell number and cytokine serum level.
abstract: OBJECTIVE
  The aim of this study was to investigate the effect of thymosin alpha 1 (TA1) on severe acute pancreatitis (SAP) in rats.
  
  
  METHODS
  Healthy Sprague-Dawley rats (n = 72) were randomly divided into four groups: control group, SAP group, and two TA1 treated groups. SAP was induced by injection of 5% sterile sodium taurocholate into the biliopancreatic duct (BPD), after which TA1 was given subcutaneously at 0 and 2 h at a dose of 100 microg/kg. The rats were killed at 3, 6 and 12 h, respectively. Serum amylase and lipase, interleukin (IL)-1beta, tumor necrosis factor-alpha (TNF-alpha), pancreatic wet/dry weight ratio and the percentage of CD3/CD4+/CD8+ T cells in peripheral blood mononuclear cells (PBMC) were measured. Next, 30 rats were randomly divided into three groups (each group containing 10 animals): SAP group (S) and two TA1 treated groups. The effects of TA1 on the survival of SAP were assessed 72 h after the induction of SAP.
  
  
  RESULTS
  There was no significant change in the serum amylase and lipase levels after TA1 administration. Levels of serum IL-1beta, TNF-alpha and pancreatic wet/dry weight ratio were significantly reduced after TA1-treatment. Application of TA1 significantly balanced CD3/CD4+/CD8+ T cells of PBMC and improved histological scores and the survival rate.
  
  
  CONCLUSIONS
  TA1 can reduce pancreatic inflammation by regulating differentiation of CD3/CD4+ T cells and decreasing the release of cytokines, thus attenuates pancreatic severity in SAP rats.
authors.affiliation: Department of Gastroenterology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
authors.forename: Weiyan
authors.initials: W
authors.lastname: Yao
authors.forename: Qi
authors.initials: Q
authors.lastname: Zhu
authors.forename: Yaozong
authors.initials: Y
authors.lastname: Yuan
authors.forename: Minmin
authors.initials: M
authors.lastname: Qiao
authors.forename: Yongping
authors.initials: Y
authors.lastname: Zhang
authors.forename: Zukang
authors.initials: Z
authors.lastname: Zhai
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D017252:CD3 Complex / Q000032:analysis; D018791:CD4 Lymphocyte Count; D016516:CD4-CD8 Ratio; D004195:Disease Models, Animal; D053583:Interleukin-1beta / Q000097:blood*; D008049:Lipase / Q000097:blood; D008168:Lung / Q000187:drug effects / Q000473:pathology; D008297:Male; D009929:Organ Size / Q000187:drug effects; D010179:Pancreas / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D010195:Pancreatitis / Q000097:blood / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012720:Severity of Illness Index; D013601:T-Lymphocytes / Q000187:drug effects* / Q000378:metabolism; D013656:Taurocholic Acid; D000077596:Thymalfasin; D013947:Thymosin / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D000893:Anti-Inflammatory Agents; D017252:CD3 Complex; D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D013656:Taurocholic Acid; D013947:Thymosin; D008049:Lipase; D000681:Amylases; D000077596:Thymalfasin