Study On The Mechanism Of Pancreatic Acinar Tissues Injury In Diabetic Rats

Objective To investigate diabetic rat pancreatic acinar tissues injury and the expressions of big mitogen activated protein kinase (big MAP kinase l, BMK1/ERK5) and inhibitor of DNA binding -2 (Id2) in pancreatic acinar tissues and their significance.methods twenty male SD rats were randomly divided into normal control group(n﹦10) and streptozotocin(STZ)-induced diabetic rat group (n﹦10). To induce diabetes, rats were treated with an intraperitoneal injection of STZ(50 mg/kg body wt) dissolved in Citrate buffer. Control rats were administered equivalent volume of Citrate buffer via the same route. On 14 weeksend,all rats were sacrificed and venous blood and pancreatic tissues were collected. Then,to detect the levels of fasting blood glucose,insulin and blood fat.The specimens of pancreas were fixed and embedded and some sections were used for morphological analysis were stained with hematoxylin-eosin and some sections were stained with periodic acid-Schiff.Some sections were used for histochemical analysis:the expressions of type I,IV collagen,platelet activating factor(PAF), tumor necrosis factor-alpha (TNF- a ) and Id2 were determined by inmmunohistochemistry and BMK1/ERK5-mRNA was determined by in situ hybridization.Results Biood fat levels were higher in diabetic group than that of control group.Compared with the control group,in diabetic group the vascular wall was thickening, inflammatory cells were infiltrated in perivascular area,local acinus was atrophy and the expression of type IV collagen was mainly expressed in vascular basement membrane , while type I collagen was in local atrophy acinus tissue with inflammation (P <0.01). Id2 was expressedin acinar and vascular endothelial cells and it's expression level in diabetic group was decreased (P <0.05). PAF, TNF-a expression levels were higher in diabetic group than that of control group (P <0.05).ERK5-mRNA was expressed in vascular endothelial cell and were significantly increased in diabetic group (P <0.01).PAS-postive materials were deposited in the vascular wall in diabetic group but were not in the control group.Conclusions Microvessel lession and chronic inflammation of pancreatic acinar tissues are caused by high expression of type of I collagen ,type of IV collagen, PAF and TNF-alpha that may be involved in high expression of ERK5 and low expression of Id2 in diabtes rats with dyslipidemia.