کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2531327 1558916 2015 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
The pro-healing effect of exendin-4 on wounds produced by abrasion in normoglycemic mice
ترجمه فارسی عنوان
اثر محافظتی اگزندین -4 بر روی زخم های ایجاد شده توسط سایش در موش های نابالغلیمی
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب سلولی و مولکولی
چکیده انگلیسی

Experimental evidence suggested that Exendin-4 (Exe4), an agonist at glucagon like receptor-1 (GLP-1R), promoted tissue regeneration. We aimed to verify the effect of Exe4, in the absence or in the presence of Exendin-4(9-39), an antagonist at GLP-1R, on the healing of abraded skin.Two wounds (approximately 1.1×1.1 cm2; namely “upper” and “lower” in respect of the head) were produced by abrasion on the back of 12 mice, which were then randomly assigned to receive an intradermal injection (20 μl) ofGroup 1: saline (NT) or Exe4 (62 ng) in the upper and lower wound respectively;Group 2: Exendin-4(9-39) (70 ng) in the upper and Exendin-4(9-39) (70 ng) and, after 15 min, Exe4 (62 ng) in the lower wound.Wounds were measured at the time of abrasion (T0) and 144 h (T3) afterward taking pictures with a ruler and by using a software. The inflammatory cell infiltrate, fibroblasts/myofibroblasts, endothelial cells and GLP-1R expression, were each labeled by immunofluorescence in each wound, pERK1/2 was evaluated by Western-blot in wound lysates.At T3, the percentage of healing surface was 53% and 92% for NT and Exe4 wounds respectively and 68% and 79% for those treated with Exendin-4(9-39) and Exendin-4(9-39)+Exe4 respectively. Exe4, but not Exendin-4(9-39) induced quantitative increase in fibroblasts/myofibroblasts and vessel density when compared to NT wounds. This increase was not evident in wounds treated with Exendin-4(9-39)+Exe4.Exe4 promotes wound healing opening to the possible dermatological use of this incretin analogue.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: European Journal of Pharmacology - Volume 764, 5 October 2015, Pages 346–352
نویسندگان
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