Establishment Of Diabetic Diabetic Corneal Model And Preliminary Study Of Epithelial Lesions

Purpose:To characterize the pathogenesis of diabetic keratopathy in a streptozocin (STZ) induced mouse model of type I diabetes mellitus (DM).Methods:Diabetes mellitus was induced via steptozocin intraperitoneal injection in C57bl/6mouse.1%rose bengal was stained on the cornea for measuring the integrity of the corneal epithelium. Corneal epithelial wound healing was determined using a vivo epithelial debridement model and compared with the age matched normal controls. Corneal morphology histology were examined by H&E staining. Oxidative stress was assessed with immunohistochemistry which marker8-oHdG. The ultrastructure of the cornea was determined with tansmission electron microscopic.Results:Compared to the normal control mouse, streptozocin mouse had showed general symptoms of diabetes:polydipsia,polyphagia, polyuria, weight loss etc. STZ mouse had a steady-state high glucose (18mmol/1), also the growth rate was lower compared with normal control mouse.1%rose bengal corneal staining had dot coloring at two weeks after STZ injection become a modle, the stained area and extent were gradually increased with the extension of the duration of diabetes, almost all the cornea was stained at16weeks after STZ injection become a modle. With the passage of time into a mold, the cornea epithelial healing time becomed longer:2weeks was about40hours;4weeks was about120hours;8,12,16weeks was about144hours; but the normal control mouse were only about48hours. Corneal epithelial cells arranged loose and polarity disappeared and edema, cell layers significantly reduced and the stroma fiber thickening derangement compared with normal control mouse. The expression of8-OHdG was higher in the corneal epithelium and superficial stroma than the normal control. Corneal epithelial had little microvilli, the number of tight junctions between epithelium cells and basement membrane were reduced significantly and so on were observed by the tansmission electron microscopic. Conclusions:The mouse were induced by STZ can be used as animal models of diabetic keratopathy (DK):the damage of epithelium for corneal and delay healing on epithelium and other symptoms. In addition, the abnormalities of epithelial in the ultrastructure and DNA oxidative stress injuryed may countributed to epithelial wound healing delay.