Involvement of Oxidative Stress in Sodium Taurocholate-Induced Acute Necrotizing Pancreatitis in Rats.
- Author:
Kyung Chul JEON
1
;
Hyung Geun LEE
;
Jong Kwon PARK
;
Jung Taik KIM
;
Jin Woo RYU
;
Dong Kook PARK
;
Min CHUNG
;
Mie Rha YANG
Author Information
1. Department of Surgery, College of Medicine, Dankook University.
- Publication Type:Original Article
- Keywords:
Free radicals;
Lipid peroxidation;
Malondialdehyde;
Glutathione;
Pancreatitis
- MeSH:
Acinar Cells;
Amylases;
Animals;
Atrophy;
Bile;
Body Weight;
Edema;
Fatty Acids, Unsaturated;
Free Radicals;
Glutathione;
Hemorrhage;
Lipid Peroxidation;
Malondialdehyde;
Metabolism;
Microscopy;
Models, Theoretical;
Oxidative Stress*;
Pancreas;
Pancreatitis;
Pancreatitis, Acute Necrotizing*;
Pancreatitis, Chronic;
Rats*;
Reactive Oxygen Species;
Sodium*;
Taurocholic Acid
- From:Journal of the Korean Surgical Society
1998;55(2):151-159
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Oxidative radicals are regarded as a major factor in the pathogenesis of both acute and chronic pancreatitis. Because oxygen radicals react most readily with polyunsaturated fatty acids, resulting in peroxidation of lipids, several studies have been performed to determine the development of lipid peroxidation in pancreatitis. The purpose of this study was to evaluate the effects of free radicals and decision of the experimental model in acute necrotizing pancreatitis. Acute necrotizing pancreatitis was induced in 18 rats by retrograde injection into the bilopancreatic duct of 2%, 3%, and 5% sodium taurocholate. After a 12-hour observation time, the pancreas / the body weight, the serum amylase and the malondialdehyde content in tissue, as well as the reduced glutathione were measured in resected tissue samples. In addition, to determine the pathologic damage grade, tissue samples were examined by light microscopy. According to the amount of sodium taurocholate injected, the serum amylase and tissue malondialdehyde concentration were significantly increased. The reduced glutathione was significantly decreased, suggesting glutathione depletion due to oxidative stress. During the 12 hours after injection the pancreatic lesions were immediate and were characterized by interstitial edema, atrophy and extensive necrotic changes of the acinar cells, and hemorrhage. The pathologic damage grade increased according to the amount of sodium taurocholate injected. This study created an experimental model for studying the pathogenesis of acute necrotizing pancreatitis by using bile acid. In acute necrotizing pancreatitis, the increased levels of lipid peroxidation products in tissues and the change in glutathione metabolism suggest ongoing peroxidation of lipids due to an enhanced generation of oxygen radicals. Therefore, antioxidant treatment can reduce tissue damage, biochemical alterations, and extrapancreatic complications, thus improving the final outcome.
