TITLE:
Effects of AGE Inhibition with Aminoguanidine in a Diabetic db/db Mouse Wound Model
AUTHORS:
Margrete Berdal, Trond Jenssen
KEYWORDS:
Diabetes, Wound, Glycation, Inhibition, Animals
JOURNAL NAME:
Journal of Diabetes Mellitus,
Vol.4 No.2,
May
6,
2014
ABSTRACT: Advanced glycation end
products (AGEs) react non-enzymatically with tissue proteins to form
irreversible structures involved in atherosclerosis, nephropathy, retinopathy,
neuropathy, and wound healing. Studies on AGE-inhibitors have demonstrated
possible prevention of diabetes complications. The present open label study was
conducted on aminoguanidine (AGu), an inhibitor of AGE-formation, to examine
potential effects on wound healing in diabetes type 2-like db/db mice 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 in
drinking 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 P = 0.01; weight-change, P = 0.04, both for linear trend across
groups 4, 2, and 3, respectively). Even so, percentage wound closure was not
improved in the AGu-treated groups compared to controls (P ≥ 0.8).