The Investigation To The Pathologic Changes Of Pancreas And Preipancretic Tissue In Hyperlipidemia Rats

Background: Hyperlipidemia is a metabolic disturbance and can induce and deteriorate life-threating acute pancreatitis, but there are few researches about the pancreas fatty or fatty accumulation or denaturalization of pancreas in heperlipidemia. We tested the pathologic changes of pancreas and peripancreatic tissue in fructose-fed rats, a model of hyperlipidemia.Methods: Sprague-Dawley Rats were divided into two groups at radmon: 1) regular rat diet (control); 2) D-fructose diet containing 60% D-fructose(FFR). After 8 weeks, blood, pancreas and peripancreas tissue were collected from each rats. The levels of monocyte chemoattractant protein-1 (MCP-1), 8-Isoprostane, malondialdehyde (MDA), nitric oxide (NO) and catalase (CAT) were tested respectively, and the expression of endothelial nitric oxide synthase (eNOS) mRNA was tested through reverse transcription polymerase reaction ( RT-PCR). The pancreas and peripancreas tissue were respectively stained by S-100 and HE.Results: The levels of MCP-1, 8-Isoprostane, MDA and NO in blood were elevated in FFR compared with those of control rats, while the level of CAT was reduced. The levels of MDA, NO and NEFA were also elevated in the FFR pancreas and peripancreas tissue. Although there were no significantly changes in the FFR pancreatic acinar cells , there existed fatty hyperplasia in the FFR pancreatic matrix and peripancreas tissue. Expression of eNOS mRNA was reduced in the FFR pancreas. Conclusion: Hyperilidemia might induce oxidative stress and fatty infiltration in pancreas and peripancreatic tissues in Sprague-Dawley Rats, which might be accounted for the pathophysiologic change in Hyperilidemic Acute Pnacreatitis (HAP).