Pancreatic fibrosis in experimental pancreatitis induced by dibutyltin dichloride

Gastroenterology. 1997 May;112(5):1664-72. doi: 10.1016/s0016-5085(97)70049-0.


Background & aims: Regulatory mechanisms in chronic pancreatitis finally resulting in pancreatic fibrosis cannot be studied sufficiently in human pancreas. Results of a new pancreatitis model in rats suitable for investigation of the processes leading to pancreatic fibrosis are presented.

Methods: Experimental pancreatitis was induced by intravenous application of 8 mg/kg body wt dibutyltin dichloride. Pancreatitis was characterized by histology, serum parameters, and immunohistochemistry, detecting inflammatory cells. Gene expression of collagen type I and transforming growth factor beta1 was shown by Northern blot analysis.

Results: Dibutyltin dichloride induced an acute edematous pancreatitis within 24 hours. Extensive infiltration with mononuclear cells could be observed after day 7 followed by the development of fibrosis. Parallel to the cell infiltration, an upregulation of messenger RNA-encoding collagen type I and transforming growth factor beta1 could be shown. An active inflammatory process could be shown until the end of the observation period, i.e., 2 months.

Conclusions: The findings suggest that dibutyltin dichloride-induced pancreatitis in rats is suitable to study cellular interactions and mediators involved in the development of pancreatic fibrosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Collagen / genetics
  • Fibrosis
  • Immunohistochemistry
  • Male
  • Organotin Compounds*
  • Pancreas / pathology*
  • Pancreatitis / blood
  • Pancreatitis / chemically induced*
  • Pancreatitis / pathology*
  • RNA, Messenger / metabolism
  • Rats
  • Transforming Growth Factor beta / genetics


  • Organotin Compounds
  • RNA, Messenger
  • Transforming Growth Factor beta
  • Collagen
  • dibutyldichlorotin