Study On The Changs Of Intestinal Motility And Interstitial Cells Of Cajal And CX43 In Diabetic Rats

Aim:To establish the models of diabetic rats and observe the alterations of interstitial cells of Cajal(ICC) and connexin43(Cx43) in proximal colonic tissue of diabetic rats and the influence of insulin intervention.Methods:Eighty-two Sprague-Dawley rats were randomly divided into three groups:normal control group,diabetic model group and insulin intervention group.Diabetes model was induced by a single intraperitoneal injection of streptozocin(STZ)(60mg/kg).The rats of normal control group and diabetic model group were killed respectively in 6 weeks、8 weeks and 10 weeks after modeling.The rats of insulin intervention group who were injected insulin glargine 8u/kg daily subcutaneously for 4 weeks after modeling 6 weeks and were killed in 10 weeks.The intestinal propulsion rate were measured by methylene blue pushing test,the expression of ICC and Cx43 in proximal colonic tissue were analyzed by immunohistochemistry.The alterations of the ultrastructure of ICC and gap junction were observed by transmission electron microscopy(TEM).Results:Compared with the control groups,the intestinal propulsion rate in diabetic rats were decreased significantly(P<0.05, P) respectively,and there has the trend of descend little by little in the diabetic groups.The intestinal propulsion rate in insulin intervention group was markedly increased(P<0.05) compared with diabetic rats.Immunohistochemical staining showed that ICC in proximal colonic tissue were densely distributed in the circular muscle layer,longitudinal muscle layer,myenteric plexus region and submucosal border.Cx43 were expressed in the submucosal border and the outer circular muscle layer.TEM show that ICC organelles degenerated,cytoplasm dissolved and the structure of gap junction loosed in diabetic rats.Compared with the diabetic group,the expression of ICC and Cx43 in proximal colonic tissue were reduced(P<0.05) with the markedly destruction of ultrastructure.Insulin intervention could accelerate the intestinal propulsion rate,increase the expression of ICC and Cx43,and reverse the ultrastructural damages.Conclusion:1.The intestinal propulsion rate is delayed in the diabetic rats,and with the duration of the extension aggravation.2.The depletion and ultrastructural damages of ICC and Cx43 may play a central role in the pathogenesis of colon dysmotility in diabetic rats.3.Insulin treatment can restored the expression and ultrastructural features of ICC and Cx43 and improve the colon dysmotility.