| Objective Ischemia-reperfusion(I/R) is a common pathophysiologic process in clinical condition.Pancreas is one of the organs most sensitive to the ischemia,which make it more vulnerable in the process of ischemia. In this study,the effect and mechanism of VEGFMCAb on the ischemic-reperfusion injury in the pancreas was determined. Methods A I/R model was built by block the celiac trunk and superior mesenteric artery with the blood vessel tongs in rats.Seventy normal male Sprague-Dawley rats were randomly divided in to three groups: Group A(control group),Group B(I/R group),Group C(VEGFMCAb treatment group).Then both group B and group C were further divided into three subgroups as the timepoint of ischemia:15min,30min.60min. Group C that was subjected to ischemia/reperfusion injury with caudal vein administration of anti-VEGFMCAb(100μg/300g) 5min before ischemia;group B with the same injury followed by saline administration in the same manner,and group A with only anesthetization leparotomy but not ischemia.Animals were killed at 6 hours after reperfusion..The expression of TNF-α,VEGF was detected by ELASA.Apoptosis of pancreatic acinar cells was examined by terminal deoxynucleotidyl transferase mediated dUTPbiot in nick end labeling(TUNEL) method. The expression of Fas,FasL mRNA and protein were detected by Real-Time PCR,Western Blot and immunohistochemistry in rat pancreatic samples.Results Compared with ischemic-reperfusion group,VEGFMCAb can significantly decrease the level of TNF-α,VEGF in serum and apoptosis index.The expression level of Fas,FasL mRNA and protein in group B was significant higher than pancreatic tissue in group treating with VEGFMCAb.In group B,Fas,FasL immunoreactivity was more intense than in corresponding VEGFMCAb treated tissue.Conclusions VEGFMCAb can protect pancreas against ischemic-reperfusion injury and can inhibit excessive apoptosis through down-regulation of Fas/FasL.
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