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 1(st) 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 1(st) and 20(th) 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.