title: Effect of baicalin on inflammatory mediator levels and microcirculation disturbance in rats with severe acute pancreatitis.
abstract: OBJECTIVE
  To investigate the effect of bacailin on inflammatory mediators and microcirculation disturbance in severe acute pancreatitis (SAP) rats and explore its therapeutic mechanism.
  
  
  METHODS
  The rats were randomly divided into SAP group, baicalin-treated group and sham operated group. At 3, 6, and 12 hours after operation, we examined the mortality rate of rats, ascites volume, and pancreatic pathological changes in each group and determined the contents of inflammatory mediators in blood as well as the changes in blood viscosity.
  
  
  RESULTS
  Compared with SAP group, treatment with baicalin is able to improve the pathological damage of the pancreas, reduce the contents of multiple inflammatory mediators in blood, decrease the amount of ascitic fluid, and reduce the mortality rates of SAP rats. The low-shear whole blood viscosity in baicalin-treated group (at 3 hours) as well as the high-shear and low-shear whole blood viscosity in baicalin-treated group (at 12 hours) were significantly lower than that in SAP group.
  
  
  CONCLUSIONS
  Baicalin has good prospects in the treatment for SAP because it can exert therapeutic effects on this disease through inhibiting the production of inflammatory mediators, decreasing blood viscosity, improving microcirculation, and mitigating the pathological damage of the pancreas.
authors: Department of General Surgery, Hangzhou First People's Hospital, Zhejiang Province, China. zxp99688@vip.163.com
authors: Xiping
authors: X
authors: Zhang
authors: Hua
authors: H
authors: Tian
authors: Chenjun
authors: C
authors: Wu
authors: Qian
authors: Q
authors: Ye
authors: Xinge
authors: X
authors: Jiang
authors: Li
authors: L
authors: Chen
authors: Yang
authors: Y
authors: Cai
authors: Rujun
authors: R
authors: Xu
authors: Wenqin
authors: W
authors: Yuan
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001201:Ascites / Q000097:blood / Q000188:drug therapy / Q000473:pathology; D015232:Dinoprostone / Q000097:blood; D005419:Flavonoids / Q000494:pharmacology*; D018836:Inflammation Mediators / Q000097:blood*; D053583:Interleukin-1beta / Q000097:blood; D008297:Male; D008833:Microcirculation / Q000187:drug effects*; D010179:Pancreas / Q000098:blood supply / Q000187:drug effects / Q000473:pathology; D010195:Pancreatitis / Q000188:drug therapy* / Q000473:pathology; D054467:Phospholipases A2 / Q000097:blood; D010972:Platelet Activating Factor / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013929:Thromboxane B2 / Q000097:blood
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D005419:Flavonoids; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D010972:Platelet Activating Factor; C038044:baicalin; D013929:Thromboxane B2; D054467:Phospholipases A2; D000681:Amylases; D015232:Dinoprostone