CAJ | 학술논문

目的研究外源性P物质(SP)对烫伤创面组织愈合及新生血管化的影响.方法 84只Wistar大鼠经腹腔一次性注射链脲佐菌素(STZ)诱导建立糖尿病大鼠模型后,于背部制备直径2 cm的深Ⅱ度烫伤创面.根据创面不同处理方式将大鼠随机分为实验组(局部注射SP)和对照组(局部注射与实验组等量的磷酸缓冲液),每组42只.分别于创面形成后当日和第1、3、7、10、14、21 天,观察创面并计算创面愈合率;免疫组织化学染色观察创面组织中新生血管内皮细胞表面标志物CD31表达,计算微血管密度.结果创面形成后第7天,实验组创面愈合率明显高于对照组,为(42.69±3.26)% vs(30.24±1.17)%(P<0.01).免疫组织化学检测发现,自创面形成后第7天起,实验组创面组织中CD31表达及微血管密度均明显高于对照组(P<0.01).结论外源性SP具有促进糖尿病烫伤创面愈合作用,其机制可能与上调创面组织中CD31表达,使新生血管再生加速有关.
목적 연구외원성P물질(SP)대탕상창면조직유합급신생혈관화적영향.방법 84지Wistar대서경복강일차성주사련뇨좌균소(STZ)유도건립당뇨병대서모형후,우배부제비직경2 cm적심Ⅱ도탕상창면.근거창면불동처리방식장대서수궤분위실험조(국부주사SP)화대조조(국부주사여실험조등량적린산완충액),매조42지.분별우창면형성후당일화제1、3、7、10、14、21 천,관찰창면병계산창면유합솔;면역조직화학염색관찰창면조직중신생혈관내피세포표면표지물CD31표체,계산미혈관밀도.결과 창면형성후제7천,실험조창면유합솔명현고우대조조,위(42.69±3.26)% vs(30.24±1.17)%(P<0.01).면역조직화학검측발현,자창면형성후제7천기,실험조창면조직중CD31표체급미혈관밀도균명현고우대조조(P<0.01).결론 외원성SP구유촉진당뇨병탕상창면유합작용,기궤제가능여상조창면조직중CD31표체,사신생혈관재생가속유관.
Objective To evaluate the effects of external substance P (SP) on scalding wound healing and neovascularization.Methods Eighty-four Wistar rats were induced into diabetic models by intraperitoneal injection of streptozotocin (STZ), and deep partial thickness scalding wound on the back with diameter of 2 cm was prepared. Rats were randomly divided into experiment group (n=42, local injection of SP) and control group (n=42, local injection of PBS). The process of wound healing was observed, and the percentages of wound closure were calculated on D0, D1, D3, D7, D10, D14, D21 post scald. The expression of CD31, surface marker of neovascular endothelial cells, was detected within the wound sites by immunohistochemical staining, and the microvessel density was calculated. Results The percentage of wound closure in experiment group was significantly higher than that in control group on D7 post scald [(42.69±3.26) % vs (30.24±1.17)%, P<0.01]. Immunohistochemical detection revealed that the expression of CD31 and the microvessel density in experiment group were significantly higher than those in control group from D7 post scald (P<0.01). ConclusionExternal SP may promote scalding wound healing in diabetic rats, the mechanism of which may be associated with upregulation of expression of CD31 and acceleration of neovascularization.