title: [Endothelial protection of tanshinone in rats of severe acute pancreatitis].
abstract: OBJECTIVE
  To investigate the protective effection of tanshinone on endothelial cells of severe acute pancreatitis (SAP) rats and the effection of tanshinone on apoptosis of aorta endothelium.
  
  
  METHODS
  Using 8% L-arginine intraperitoneal to inject in rats, 4.4 mg/g per time, repeat injection 1 hour later, for establishing SAP model. Model rats were randomly divided into SAP group and tanshinone group. 20 mg/kg Sodium Tanshinon II Asilate i. p. was applied to tanshinone group,while the saline was used to replace Sodium Tanshinon II Asilate in SAP group. Twelve rats of each group were sacrificed at 12 h, 24 h after treatment. The pathological changes in pancreatic tissues were observed. Abdominal aorta samples were collected for terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling (TUNEL) and reverse transcription PCR (RT-PCR) tests. The blood samples were collected from abdominal aorta for analysis. Detections: (1) The concentration of Von Willebrand factor (vWF), soluble endothelial protein C receptor (sEPCR), tumor necrosis factor alpha (TNF-alpha) and the serum levels of nitric oxide (NO) were quantitative messured by ELISA. (2) The apoptosis of aorta endothelium cell was examined using TUNEL method. (3) Bcl-2 and Bax mRNA expression were measured by RT-PCR.
  
  
  RESULTS
  The pathological changes of pancreatic tissues were more severe in SAP group than those in tanshinone group. Compared with SAP group, treatment with tanshinone effectively inhibited TNF-alpha (P < 0.05), vWF (P < 0.05) and sEPCR (P < 0.05) expression and depressed apoptosis of aorta endothelium cell, increased the expression of Bcl-2 mRNA (P < 0.05), Bcl-2 mRNA/Bar mRNA ratio (P < 0.05) and the expression of Bax mRNA (P < 0.05) were decreased significantly.
  
  
  CONCLUSIONS
  Sodium Tanshinon II Asilate can lighten the SAP rats aortic endothelial injury and apoptosis of endothelial cells can reduce endothelial damage of SAP rats by TNF-alpha expression suppression.
authors.forename: Ning
authors.initials: N
authors.lastname: Ge
authors.forename: Zhi
authors.initials: Z
authors.lastname: Zeng
authors.forename: Zi-Qi
authors.initials: ZQ
authors.lastname: Lin
authors.forename: Zhong-Hua
authors.initials: ZH
authors.lastname: Yang
authors.forename: Qing
authors.initials: Q
authors.lastname: Xia
mesh_terms: D045784:Abietanes / Q000494:pharmacology*; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000473:pathology; D017209:Apoptosis; D001779:Blood Coagulation Factors / Q000378:metabolism; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000473:pathology; D009569:Nitric Oxide / Q000097:blood; D010179:Pancreas / Q000187:drug effects / Q000473:pathology; D010195:Pancreatitis / Q000188:drug therapy*; D051381:Rats; D011956:Receptors, Cell Surface / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D045784:Abietanes; D001779:Blood Coagulation Factors; D011956:Receptors, Cell Surface; D014409:Tumor Necrosis Factor-alpha; C091963:activated protein C receptor; D014841:von Willebrand Factor; C021751:tanshinone; D009569:Nitric Oxide