Gut Liver.
2011 Dec;5(4):513-520.
Heat Shock Proteins and Autophagy in Rats with Cerulein-Induced Acute Pancreatitis
- Affiliations
-
- 1Division of Gastroenterology, Department of Internal Medicine, Seoul Paik Hospital, Inje University College of Medicine, Seoul, Korea.
- 2Division of Gastroenterology and Hepatology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea. hslee60@korea.ac.kr
- 3Department of Anatomy, Chosun University School of Medicine, Gwangju, Korea.
- 4Department of Anatomy, Jeju National University School of Medicine, Jeju, Korea.
Abstract
- BACKGROUND/AIMS
Heat shock proteins (HSPs) protect rats from cerulein-induced acute pancreatitis (AP) by preventing the subcellular redistribution of cathepsin B and the activation of trypsinogen. Autophagy plays a critical role in the secretion of digestive enzymes and triggering of cerulein-induced AP via the colocalization of trypsinogen and lysosomes. Therefore, using a rat cerulein-induced AP model, we investigated whether HSPs prevent AP by regulating autophagy.
METHODS
Twelve hours after fed standard laboratory chow and water, the experimental groups (cerulein, water-immersion [WI]-cerulein and heat-shock [HS]-cerulein) and the control groups (control, WI, and HS) received one intraperitoneal injection of cerulein (50 microg/kg) or saline, respectively. All of the rats were sacrificed at 6 hours after injection. The severity of the AP was assessed based on the serum amylase level and the histological and electron microscopy findings. Western blotting was also performed for HSP60/70 and LC3B-II.
RESULTS
WI and HS induced HSP60 and HSP70, respectively. The induced HSP60/70 effectively prevented the development of cerulein-induced AP. Autophagy developed in the rats with cerulein-induced AP and was documented by the expression of LC3-II and electron microscopy findings. The WI-stressed rats and HS-treated rats did not develop cerulein-induced autophagy.
CONCLUSIONS
HSPs exert protective effects against cerulein-induced AP in rats by inhibiting autophagy.
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