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Advanced glycation end products (AGEs) react non-enzymatically with tissue proteins to form irreversiblestructures involved in atherosclerosis, nephropathy, retinopathy, neuropathy, andwound healing. Studies on AGE-inhibitors have demonstrated possible prevention of diabetescomplications. The present open label study was conducted on aminoguanidine (AGu), an inhibitorof AGE-formation, to examine potential effects on wound healing in diabetes type 2-like db/dbmice during 5 - 6 weeks. The animals were divided into 4 groups: AGu from the day of wounding(day 0) topically and/or systemically in drinking water (1 g/L; group 1, n = 13); AGu 1 g/L indrinking water from 7 weeks prior to day 0 (group 2, n = 21); AGu 5 g/L in drinking water from 9 -11 weeks prior to day 0 (group 3, n = 6); placebo controls (group 4, n = 8). Results: Glycated hemoglobin(A1C) was significantly lower in group 3 compared to the other groups (P < 0.05). Percentagechange in A1C and body weight from baseline to the end of the experiment were both relatedto the AGu doses (1 or 5 g/L; A1C-change, P = 0.01; weight-change, P = 0.04, both for lineartrend across groups 4, 2, and 3, respectively). Even so, percentage wound closure was not improvedin the AGu-treated groups compared to controls (P ≥ 0.8)

Effects of AGE Inhibition with Aminoguanidine in a Diabetic &lt;i&gt;db/db&lt;/i&gt; Mouse Wound Model

Effects of AGE Inhibition with Aminoguanidine in a Diabetic <i>db/db</i> Mouse Wound Model