Department of Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Price Institute of Surgical Research, University of Louisville, and Noveratech LLC of Louisville, United States.
Price Institute of Surgical Research, University of Louisville, and Noveratech LLC of Louisville, United States.
Acta Histochem. 2021 Feb;123(2):151680. doi: 10.1016/j.acthis.2021.151680. Epub 2021 Jan 11.
Random skin flap (RSF) is commonly used in plastic and reconstructive surgery, but its distal part often occurs ischemia. Type 1 Diabetes mellitus (T1DM), may be detrimental for flap survival by provide sever ischemia. We sought to determine the influence of DM on the relation between mast cells and angiogenesis by examining tryptase and Fms-like tyrosine kinase 1 (Flt-1), a well-known vascular endothelial growth factor receptor (VEGFR-1), in the surviving areas of RSF in healthy and diabetic rats. 16 male rats divided into healthy and diabetic groups. T1DM was created in the diabetic rats, followed by generation of a RSF in both the control and diabetic rat. On day 7, the surviving areas of each RSF were recorded. Then animals were euthanized, and numbers of vessels, mast cells and co-localization of mast cell tryptase and Flt-1 were analyzed. T1DM decreased survival areas in the RSF compared to the healthy rats, with higher percentage of intact and degranulated mast cells. T1DM elevated the expression percentage of tryptase and VEGFR-1in the proximal and middle areas of the survival parts of the RSF in most diabetic rats. Generally, our results showed that mast cell degranulation might have a positive correlation with VEGFR-1 and in this current model of ischemic tissue in diabetic rats, this finding could lead to poor angiogenesis and weakened blood vessel function, which might result in decreased RSF survival. Additional molecular mechanisms that pertain to the effects of DM on ischemic tissues healing such as this RSF model should be determined by further investigations.
随机皮瓣（RSF）常用于整形和重建手术，但皮瓣的远端部分常发生缺血。1 型糖尿病（T1DM）可能通过提供严重的缺血对皮瓣存活产生不利影响。我们试图通过检查健康和糖尿病大鼠 RSF 存活区的类胰蛋白酶和 Fms 样酪氨酸激酶 1（Flt-1），即众所周知的血管内皮生长因子受体（VEGFR-1），来确定糖尿病对肥大细胞与血管生成之间关系的影响。将 16 只雄性大鼠分为健康组和糖尿病组。在糖尿病大鼠中建立 T1DM，然后在对照组和糖尿病大鼠中生成 RSF。第 7 天，记录每个 RSF 的存活面积。然后处死动物，分析血管、肥大细胞的数量以及肥大细胞类胰蛋白酶和 Flt-1 的共定位。与健康大鼠相比，T1DM 降低了 RSF 的存活面积，且完整和脱颗粒肥大细胞的百分比更高。T1DM 增加了大多数糖尿病大鼠 RSF 存活部分近端和中部区域的类胰蛋白酶和 VEGFR-1 的表达百分比。总的来说，我们的结果表明肥大细胞脱颗粒可能与 VEGFR-1 呈正相关，在这种糖尿病缺血组织的当前模型中，这一发现可能导致血管生成不良和血管功能减弱，从而导致 RSF 存活减少。应该通过进一步的研究来确定与糖尿病对缺血组织愈合的影响相关的其他分子机制，例如这种 RSF 模型。
