Objective To investigate the effects of cimetidine on the red cell immune function and interleukin-2(IL-2) in rats with obstructive jaundice. Methods Sixty SD rats were divided into bile duct ligation(BDL) group, cimetidine therapy (BDLC) group and sham operation(SO) group respectively. The red cell immue function and serum IL-2 level were determined with the red cell yeast-rosttes test and radioimmunoassay respectively. Results The red blood cell C3b receptor rosette rate(RBC-C3bRR), the red blood cell immune complex rosette rate(RICR), the red blood cell C3b receptor rosette-forming excited rate(RFER) and serum IL-2 level were significantly lower in BDL group as compared with SO group, the red blood cell C3b receptor rosette-forming inhibitory rate(RFIR) in BDL group was higher than that of SO group. After 7 days’ cimetidine therapy RBCC3bRR, RICR, RFER and IL-2 became higher than those of BDL group, but RFIR was lower than that of BDL group. Conclusion Supplemental cimetidine can significantly enhance the impaired red cell immune function and IL-2 production in rats with obstructive jaundice.
【Abstract】ObjectiveTo investigate the effect of ischemia-reperfusion （I/R） injury on apoptosis of pancreatic cells in rats with acute pancreatitis(AP). MethodsFifty-four SD rats were randomized into 3 groups: pancreatitis group (n=24), I/R-injury group (n=24) and control group (n=6). The animal model of AP was induced by retrograde injection of 3% sodium taurocholate into biliopancreatic duct in rats. Pancreatic I/R was caused by blocking the inferior splenic artery and removing the clamp after AP induction. At 1 h, 3 h, 6 h and 12 h, groups of rats were sacrificed. A terminal deoxynucleotidyl transferase-mediated dUTP-biotion nick end labeling (TUNEL) was used to detect pancreatic apoptosis, and histological changes of the pancreas were observed. ResultsPancreatic hemorrhage, necrosis were respectively observed in the pancreatitis rats at 6 h and the I/R-injury rats at 1 h. Histological changes of the pancreatitis rats at 1 h and 3 h were only congestion and edema. Apoptoic acinar cells increased after AP induction, the peak respectively appeared at 6 h in the pancreatitis rats and at 3 h in the I/R-injury rats. Compared with the pancreatitis rats, apoptosis index (AI) of the I/Rinjury rats was significantly higher at 1 h and 3 h (P＜0.01, P＜0.05, respectively), but lower at 6 h and 12 h (P＜0.05, P＜0.01, respectively). ConclusionI/R injury can induce conversion of edematous pancreatitis to hemorrhagic necrotizing pancreatitis and apoptosis of acinar cells. Apoptosis may be a beneficial response to pancreatic injury in AP.