Abstract
The present study was undertaken to study the role of PAR-2 receptor activation in pathophysiology of intestinal inflammation. Inflammatory bowel disease was induced in Wistar albino rats by intrarectal administration of 2, 4, 6 trinitrobenzenesulfonic acid (TNBS, 0.25 ml 120 mg/ml in 50% ethanol intrarectally, on 1st day only). Trypsin (500 μg/kg, 1 mg/kg, 5 mg/kg, intrarectal) was given from the same day up to 20 days. Various physical parameters including body weight, food and water intake were measured on 1st and 20th days. At end of the experiment, colon weight and various histopathological indexes were assessed. The colon homogenate malondialdehyde (MDA), myeloperoxidase (MPO), and superoxide dismutase (SOD) and % mast cell protection in mesentery were also measured. Trypsin at higher dose (5 mg/kg) showed the higher level of oxidative enzymes and lower level of protective enzymes as compared to the animals treated with only TNBS. Trypsin treatment produced significantly more mast cell degranulation. Finally in the histopathology, there was increased in severity of the disease in trypsin-treated animals. The role of PAR-2 (protease activated receptor-2) receptor in gut is pro-inflammatory and thus appears as a new potential therapeutic target for inflammatory bowel disease treatments.
Highlights
Inflammatory bowel disease encompasses a number of chronic, relapsing inflammatory disorders involving the gastrointestinal tract.[1]
Group 3: TNBS (0.25 ml, 120 mg/ml in 50% ethanol, intrarectally) on 1st day only 1 Trypsin (5 mg/kg, intrarectal) treatment continued till 20th day; TNBS was delivered by a Teflon cannula through the anus of each rat
TNBS is a hapten compound, and when it is bound with a substance of high molecular tissue proteins, it will turn In inflammatory bowel disease (IBD), body weight, food intake, and water intake are the important indicators of the severity of this disease
Summary
Inflammatory bowel disease encompasses a number of chronic, relapsing inflammatory disorders involving the gastrointestinal tract.[1]. The intestine (bowel) becomes inflamed, often causing recurring abdominal cramps and diarrhea. The exact cause of ulcerative colitis remains undetermined, the condition appears to be related to a combination of genetic and environmental factors. While not one factor has been identified as the initial trigger for inflammatory bowel disease.[2] Proteinase-activated receptors (PARs) have the common property of being activated by the proteolytic cleavage of their extracellular N-terminal domain. The new NH22 terminus acts as a ‘tethered ligand’ binding and activating the receptor itself. Four members of this family have been cloned, three of which are activated by thrombin
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