Suckow Mark A, Gobbett Troy A, Peterson Richard G
Department of Veterinary Population Medicine, University of Minnesota, St. Paul, MN, U.S.A.
PreClinOmics, Inc., Indianapolis, IN, U.S.A.
In Vivo. 2017 Jan 2;31(1):55-60. doi: 10.21873/invivo.11025.
Animal models of diabetic delayed wound healing are essential to the development of strategies to improve clinical approaches for human patients. The Zucker diabetic Sprague Dawley (ZDSD) rat has proved to be an accurate model of diet-induced obesity and diabetes and we evaluated the utility of the ZDSD rat as a model for delayed wound healing associated with diabetes and obesity. Groups of ZDSD and Sprague Dawley (SD) rats were placed on a diabetogenic diet and evaluated two weeks later for hyperglycemia, as a sign of diabetes. Rats with blood glucose levels of >300 mg/dl were considered diabetic and those with blood glucose of <180 mg/dl were considered non-diabetic. All SD rats were non-diabetic. A full-thickness excisional skin wound was created in anesthetized rats using a punch biopsy and wound diameter measured on days 1, 4, 7, 9 and 11. Blood glucose levels and body weights were measured periodically before and after wounding. Diabetic ZDSD rats had significantly greater blood glucose levels than non-diabetic ZDSD and SD rats within 10 days of being placed on the diabetogenic diet. Furthermore, diabetic ZDSD rats initially weighed more than non-diabetic ZDSD and SD rats, however, by the end of the study there was no significant difference in body weight between the ZDSD groups. By day nine, wounds in ZDSD rats were significantly larger than those in SD rats and this persisted until the end of the study at day fourteen. Wounds from all groups were characterized histologically by abundant fibroblast cells, collagen deposition and macrophages. These results demonstrate delayed wound healing in both diabetic and non-diabetic ZDSD rats and suggest that obesity or metabolic syndrome are important factors in wound healing delay.
糖尿病延迟伤口愈合的动物模型对于开发改善人类患者临床治疗方法的策略至关重要。Zucker糖尿病斯普拉格-道利(ZDSD)大鼠已被证明是饮食诱导的肥胖和糖尿病的准确模型,我们评估了ZDSD大鼠作为与糖尿病和肥胖相关的延迟伤口愈合模型的效用。将ZDSD和斯普拉格-道利(SD)大鼠分组置于致糖尿病饮食中,两周后评估高血糖情况,作为糖尿病的标志。血糖水平>300mg/dl的大鼠被认为患有糖尿病,血糖<180mg/dl的大鼠被认为非糖尿病。所有SD大鼠均非糖尿病。使用打孔活检在麻醉的大鼠身上制造全层切除性皮肤伤口,并在第1、4、7、9和11天测量伤口直径。在伤口前后定期测量血糖水平和体重。在给予致糖尿病饮食的10天内,糖尿病ZDSD大鼠的血糖水平明显高于非糖尿病ZDSD大鼠和SD大鼠。此外,糖尿病ZDSD大鼠最初体重比非糖尿病ZDSD大鼠和SD大鼠重,然而,到研究结束时,ZDSD组之间的体重没有显著差异。到第9天,ZDSD大鼠的伤口明显大于SD大鼠的伤口,这种情况一直持续到研究结束的第14天。所有组的伤口在组织学上的特征是有成纤维细胞、胶原蛋白沉积和巨噬细胞。这些结果表明糖尿病和非糖尿病ZDSD大鼠的伤口愈合均延迟,并表明肥胖或代谢综合征是伤口愈合延迟的重要因素。