Published online Jan 15, 2003. doi: 10.3748/wjg.v9.i1.160
Revised: July 23, 2002
Accepted: August 5, 2002
Published online: January 15, 2003
AIM: To study the expression of neurokinin-1 receptor (NK-1R) and neurokinin-2 receptor (NK-2R) in distal ileum of acute necrotizing pancreatitis (ANP) and to evaluate the relationship between expression of these two receptors and intestinal mucosal damage.
METHODS: A total of 130 adult Sprague-Dawley rats were randomly divided into two groups: the rats in ANP group (n = 80) were induced by the retrograde intraductal infusion of 30 g·L-1 sodium taurocholate. And the rats in normal control group (n = 50) received laparotomy only. Sacrifices were made 6 h, 12 h, 24 h and 48 h later in ANP and normal control group after induction respectively. Intestinal mucosal permeability was studied by intrajejunal injection of 1.5mCi radioactive isotope 99mTc-diethlene triamine pentacetic acid (DTPA) and the radioactivity of 99mTc-DTPA content in urine was measured 6 h, 12 h, 24 h and 48 h after induction. Then the pancreas and intestine were prepared for pathology. Reverse transcription polymerase chain reaction (RT-PCR) was used to determine the mRNA expression of NK-1R and NK-2R, and Western blot was used to investigate the protein level of NK-1R and NK-2R.
RESULTS: In ANP rats, serious histologic damages in intestinal mucosa were observed, and the radioactivity of 99mTc-DTPA in urine increased significantly in the ANP group. RT-PCR revealed that NK-1R and NK-2R mRNA level was overexpressed in the distal ileum of ANP as compared with the normal control group. Western blot discovered stronger NK-1R (14-fold increase) and NK-2R (9-fold increase) immunoreactivity in the intestinal mucosa of ANP rats. Moreover, the overexpression of NK-1R was associated with mucosal pathological score (r = 0.77, P < 0.01) and intestinal permeability (r = 0.68, P < 0.01) in ANP rats.
CONCLUSION: NK-1R and NK-2R contribute to disrupted neuropeptides loop balance, deteriorate intestinal damage, and are involved in pathophysiological changes in ANP.