Effect of C-peptide on Cognitive Dysfunction and Neuronal Apoptosis Caused by beta amyloid 1-42 in Diabetic Rats

Abstract

Background & Aim: Alzheimer disease is characterized by a progressive loss of memory. Its prevalence in diabetic patients is nearly twice in comparison of others. Recent findings suggest that C-peptide replacement in type 1 diabetes exerts beneficial effects on diabetic rats. We examined the effects of C-peptide on cognitive dysfunction and neuronal apoptosis caused by Aβ 1-42 on working memory in Streptozotocin induced diabetic rats. Methods: In the present experimental study which was carried out in 2009 at Shiraz University of Medical Sciences, 50 male Sprague Dawley rats (230-300 gr) were divided into five groups: control, type 1 diabetic, diabetic groups receiving C-peptide, diabetic group receiving beta amyloid, diabetic group receiving beta amyloid and c-peptide. The Neuronal apoptosis were assessed with tunnel staining. Diabetes was induced with IV injection of Streptozotocin (60 mg/kg). Twenty six days after the onset of diabetes, behavioral tests were conducted for three days. For data analysis, the Tukey and One way ANOVA tests were used. Results: In comparison to control group, in all diabetic groups working memory impairments was observed (P<0.05), but Aβ 1-42 caused severe deficits in the working memory (P<0.001) and C-peptide could significantly decrease the impairment (P<0.05). Only the diabetic beta amyloid group showed significant amount of tunnel positive neuron (P<0.05) and c-peptide replacement significantly decreased the amount of these cells (P<0.05). Conclusion: C-peptide could significantly decrease memory impairment and neuronal apoptosis among diabetic rats