Effect of baicalin on inflammatory mediator levels and microcirculation disturbance in rats with severe acute pancreatitis

Pancreas. 2009 Oct;38(7):732-8. doi: 10.1097/MPA.0b013e3181ad9735.

Abstract

Objectives: 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Amylases / blood
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Ascites / blood
  • Ascites / drug therapy
  • Ascites / pathology
  • Dinoprostone / blood
  • Flavonoids / pharmacology*
  • Inflammation Mediators / blood*
  • Interleukin-1beta / blood
  • Male
  • Microcirculation / drug effects*
  • Pancreas / blood supply
  • Pancreas / drug effects
  • Pancreas / pathology
  • Pancreatitis / drug therapy*
  • Pancreatitis / pathology
  • Phospholipases A2 / blood
  • Platelet Activating Factor / metabolism
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Thromboxane B2 / blood

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Flavonoids
  • Inflammation Mediators
  • Interleukin-1beta
  • Platelet Activating Factor
  • baicalin
  • Thromboxane B2
  • Phospholipases A2
  • Amylases
  • Dinoprostone