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AIM:To study the expression of neurokinin-1 receptor(NK-1R)and neurokinin-2 receptor(NK-2R)in distal ileum ofacute necrotizing pancreatitis(ANP)and to evaluate therelationship between expression of these two receptors andintestinal mucosal damage.METHODS:A total of 130 adult Sprague-Dawley rats wererandomly divided into two groups:the rats in ANP group(n=80)were induced by the retrograde intraductal infusionof 30 g·L~(-1)sodium taurocholate.And the rats in normal controlgroup(n=50)received laparotomy only.Sacrifices weremade 6 h,12 h,24 h and 48 h later in ANP and normalcontrol group after induction respectively.Intestinal mucosalpermeability was studied by intrajejunal injection of 1.5mCiradioactive isotope ~(99m)Tc-diethlene triamine pentacetic acid(DTPA)and the radioactivity of ~(99m)Tc-DTPA content in urinewas measured 6 h,12 h,24 h and 48 h after induction.Then the pancreas and intestine were prepared forpathology.Reverse transcription polymerase chain reaction(RT-PCR)was used to determine the mRNA expression ofNK-1R and NK-2R,and Western blot was used to investigatethe protein level of NK-1R and NK-2R.RESULTS:In ANP rats,serious histologic damages inintestinal mucosa were observed,and the radioactivity of~(99m)Tc-DTPA in urine increased significantly in the ANP group.RT-PCR revealed that NK-1R and NK-2R mRNA level wasoverexpressed in the distal ileum of ANP as compared withthe normal control group.Western blot discovered strongerNK-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 withmucosal pathological score(r=0.77,P<0.01)and intestinalpermeability(r=0.68,P<0.01)in ANP rats.CONCLUSION:NK-1R and NK-2R contribute to disruptedneuropeptides loop balance,deteriorate intestinal damage,and are involved in pathophysiological changes in ANP.
AIM: To study the expression of neurokinin-1 receptor (NK-1R) and neurokinin-2 receptor (NK-2R) in distal ileum ofacute necrotizing pancreatitis (ANP) and to evaluate therelationshipbetween expression of these two receptors andintestinal 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 of each.Intestinal mucosalpermeability was studied by intrajejunal injection of 1.5 m Ciradioactive isotope ~ (99m) Tc- diethlene triamine pentacetic acid (DTPA) and the radioactivity of ~ (99m) Tc-DTPA content in urine was measured 6 h, 12 h, 24 h and 48 h after induction. The pancreas and intestine were prepared for pathology. (RT-PCR) was used to determine the mRNA expression ofNK-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 inintestinal mucosa were observed, and the radioactivity of ~ ( 99m) Tc-DTPA in urine increased significantly in the ANP group. RT-PCR revealed that NK-1R and NK-2R mRNA level wasoverexpressed in the distal ileum of ANP as compared with the normal control group. Western blot was found strongerNK-1R -fold increase) and NK-2R (9-fold increase) immunoreactivity in the intestinal mucosa of ANP rats. Moreover, the overexpression of NK-IR was associated with mucosal pathological score (r = 0.77, 0.68, P <0.01) in ANP rats. CONCLUSION: NK-1R and NK-2R contribute to disrupted loops of balance, deterstinal intestinal damage, and are involved in pathophysiological changes in ANP.