Expression of NOD2 in a Rat Model of Acute Pancreatitis
ABSTRACT To observe the expression of nucleotide-binding oligomerization domain 2 (NOD2) in rats with acute pancreatitis (AP).
Sprague-Dawley rats were randomly divided into sham operation (SO) groups and AP groups. Acute pancreatitis was induced with retrograde infusion of sodium taurocholate into the biliopancreatic duct. They were then killed at 3, 6, 12, 24, and 48 hours after induction of AP. Blood biochemical indicators were detected with automatic biochemistry analyzer. Nuclear factor-κB (NF-κB) was measured by immunohistochemistry. The NOD2 was detected by real-time quantitative polymerase chain reaction and Western blot. Tumor necrosis factor-α (TNF-α) was determined by enzyme-linked immunosorbent assay.
Compared with the SO group, the level of messenger RNA and protein of NOD2 in pancreatic tissue and peritoneal white blood cells (PWBCs) in the AP groups significantly declined (P < 0.05). The messenger RNA level of NOD2 in the AP groups was correlated positively with amylase (P < 0.05) and negatively with TNF-α (P < 0.05); TNF-α significantly decreased in the AP groups, whereas NF-κB significantly increased (P < 0.05).
The NOD2 may play an important role in the up-regulation and activation of NF-κB during inflammation reactions in AP.
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ABSTRACT: Laboratory animals are used and the experimental research is run in various scientific fields such as human and animal health, disease control, sustainable environmental health, health industry and product innovation, and biosafety planning. The experimental research includes those studies that are not yet proven to be completely safe or those not possible to be run on humans. Rats, mice and rabbits are commonly used in these studies. Based on the kind of the study, cats, dogs, guinea pigs, hamsters, sheep, cattle, chicken, sparrows, goats, horses, nonhuman primates, invertebrates, fish and fly species can be used. Though labaratory animals provide significant contributions to the humans and development in science, they require protection by humans and require to be protected from unfair use. Ethical boards and rules are formed to accomplish those goals prohibited the use of the laboratory animals in experimental research under unethical conditions and ruled that any research shall use methods that require the least amount of pain and suffering. The boards ruled not only on research methods but also on feeding and management practices to uphold the main principles of animal welfare. It is obvious that these rulings are the already late responsibility of human kind.
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ABSTRACT: Acute pancreatitis (AP) is a formidable disease, which, in severe forms, causes significant mortality. Biliary AP, or gallstone obstruction-associated AP, accounts for 30-50% of all clinical cases of AP. In biliary AP, pancreatic acinar cell (PAC) death (the initiating event in the disease) is believed to occur as acinar cells make contact with bile salts when bile refluxes into the pancreatic duct. Recent advances have unveiled an important receptor responsible for the major function of bile acids on acinar cells, namely, the cell surface G-protein-coupled bile acid receptor-1 (Gpbar1), located in the apical pole of the PAC. High concentrations of bile acids induce cytosolic Ca(2+) overload and inhibit mitochondrial adenosine triphosphate (ATP) production, resulting in cell injury to both PACs and pancreatic ductal epithelial cells. Various bile salts are employed to induce experimental AP, most commonly sodium taurocholate. Recent characterization of taurolithocholic acid 3-sulphate on PACs has led researchers to focus on this bile salt because of its potency in causing acinar cell injury at relatively low, sub-detergent concentrations, which strongly implicates action via the receptor Gpbar1. Improved surgical techniques have enabled the infusion of bile salts into the pancreatic duct to induce experimental biliary AP in mice, which allows the use of these transgenic animals as powerful tools. This review summarizes recent findings using transgenic mice in experimental biliary AP.HPB 02/2012; 14(2):73-81. DOI:10.1111/j.1477-2574.2011.00408.x · 2.05 Impact Factor