大鼠急性β射线皮肤损伤创面愈合过程中Ang-1及其受体的表达

摘要

目的 探讨急性β射线皮肤损伤创面难愈合过程中血管生成素1(Ang-1)及其受体Tie-2表达的动态变化.方法 雌性大鼠54只分为3组:照射组(n=24),直线加速器产生β射线(45 Gy)单次照射大鼠臀部皮肤40 mm×40 mm,建立急性β射线皮肤损伤模型;烧伤组(n=24),以直径为25mm的恒温电烙铁,温度80℃,时间8s,建立大鼠深Ⅱ度热力烫伤动物模型;对照组(n=6),正常大鼠.取不同时期创面皮肤组织,采用免疫组化SP法及RT-PCR等方法,检测1、2、3、4周不同时相点各组大鼠创面组织中Ang-1蛋白、Tie-2蛋白和Ang-1 mRNA、Tie-2 mRNA的表达.结果 正常大鼠皮肤中Ang-1、Tie-2积分吸光度(A)值低表达;照射组伤后1、2和3周的Ang-1 A值分别为0.130±0.012、0.170±0.013和0.192±0.072,明显低于烧伤组的0.190±0.182、0.332±0.014和0.273±0.014(P＜0.05);照射组1、2和3周的Tie-2 A值分别为0.112±0.011、0.183±0.012和0.171±0.061,亦明显低于烧伤组的0.170±0.062、0.310±0.013和0.284±0.014 (P＜0.05);Ang-1 mRNA、Tie-2mRNA表达的变化与Ang-1蛋白、Tie-2蛋白相似.结论 急性β射线皮肤损伤创面愈合过程中,Ang-1及Tie-2持续低表达可能是急性β射线皮肤损伤创面难愈合的机制之一.%Objective To investigate the dynamic expressions of angiopoietin 1 (Ang-1) and its receptor Tie-2 in acute β-ray-irradiated skin injury. Methods Fifty-four female SD rats were divided into 3 groups. The models of acute (3-ray-irradiated skin injury were established by radiation with 45 Gy fi-ray on the skin in 24 ratsCgroup A). The models of deep second degree burn were established by electrical scald instrument with constant temperature 80℃,8 s and 25 mm as common traumatogenic factors in 24 rats(group B). Six normal rats were served as normal controls (group C). The expressions of Ang-1 and Tie-2 proteins and Ang-1 mRNA and Tie-2 mRNA were semi-quantitatively checked by immunohistochemical SP technique and RT-PCR, respectively at 1,2 and 3 weeks after radiation, Results Lower expressions of Ang-1 and Tie-2 proteins were identified in rat skin in group C. The Ang-1 absorbance values of 1,2 and 3 weeks in group A were 0. 130 ± 0. 012,0. 170±0. 013 and 0. 192±0. 072,which were lower than 0. 190±0. 182,0. 332 ± 0. 014 and 0. 273 ± 0. 014 in group B(P<0. 05). The Tie-2 absorbance values of 1,2 and 3 weeks in group A were 0.112±0.011,0. 183 +0.012 and 0. 171 ± 0. 061,which were lower than 0. 170±0.062,0.310 ± 0.013 and 0.284 ± 0.014 in group B(P<0. 05). The changes of Ang-1 mRNA and Tie-2 mRNA were similar to those of Ang-1 and Tie-2 proteins. Conclusion The persisting lower expressions of Ang-1 and Tie-2 may be one of the mechanisms involved in the of retarded healing of acute j3-ray radiation injured skin wounds.