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Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice
Published on: June 28, 2021
Pathogenesis of acute pancreatitis
1Department of Surgery, Charles A. Dana Research Laboratories, Boston, Massachusetts.
Annual Review of Medicine
|January 1, 1988
Summary
Blocking digestive enzyme secretion in pancreatic acinar cells may cause acute pancreatitis. This occurs when enzymes activate within the cell, initiating a harmful cascade.
Area of Science:
- Gastroenterology
- Cell Biology
- Pathophysiology
Background:
- Acute pancreatitis pathogenesis is not fully understood.
- Recent studies implicate acinar cell dysfunction.
Purpose of the Study:
- To investigate the role of blocked digestive enzyme secretion in acinar cells in acute pancreatitis.
- To explore the intracellular mechanisms leading to pancreatitis.
Main Methods:
- Utilized experimental models of acute pancreatitis.
- Examined the localization of digestive enzymes and lysosomal hydrolases.
- Investigated the activation of trypsin within intracellular vacuoles.
Main Results:
- Digestive enzymes were found co-localized with lysosomal hydrolases in intracellular vacuoles.
- Cathepsin B mediated trypsin activation within these vacuoles.
- This activation initiates a cascade of zymogen activation.
Conclusions:
- Events within pancreatic acinar cells, specifically blocked enzyme secretion and subsequent intracellular activation, are critical in initiating acute pancreatitis.
- Pancreatitis development may originate intracellularly, rather than in the ductal system or interstitium.
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