Type 1 diabetes (T1D) is a syndrome that upsurges the autoimmune destruction of insulin-producing pancreatic β cells. This study aims at investigating the potential and protective role of caffeic acid phenethyl ester (CAPE) on T1D experimental model. Swiss mice were assigned into three groups of eight mice/group. Group 1 mice were normal; Groups 2 is induced diabetic mice by administration of cyclosporin/STZ and group 3 is a diabetic mice treated with CAPE6 µM/kg. Mice group 2 showed marked increases in blood glucose levels. As regard to glycogen hepatic content, a 35.3% reduction was observed in the induced diabetic group 2, this reduction improved to 1.5% in treated group 3. Consequently, a significant elevation of SOD, GSH, and CAT enzymes were seen in the treated group compared to untreated. In addition, serum MMP-9 significantly reduced and TMP-1 appeared to have significantly increased in the treated group compared with untreated. Furthermore, histopathological examination showed marked regenerative changes and normal architecture of islet cell in the treated group compared with untreated once. CAPE has antidiabetic properties related to their anti-inflammatory and angiogenic inhibitor activation effects and may be relevant in the future for human diabetic therapy.
 

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