650nm低能量半导体激光对兔耳皮肤全层损伤修复的作用

Repair Effect of 650nm Low Energy Semiconductor Laser on Full-thickness Skin Injury in Rabbit Ear

目的探讨650 nm低能量半导体激光对兔耳皮肤全层损伤的修复作用及机制。方法在SPF级兔耳制作2 cm×2 cm正方形全层皮肤损伤模型,造模第11天开始:对照组每天用生理盐水清洗伤口,试验组生理盐水清洗创面后进行650 nm的低能量半导体激光照射治疗。观察两组的创面愈合时间、挛缩指数、白细胞计数、组织形态学改变及血管内皮细胞生长因子(vascular endothelial growth factor,VEGF)的表达差异。结果试验组和对照组创面愈合时间平均是(23.79±3.75)d和(26.68±4.35)d;挛缩指数分别为0.09±0.43和0.22±0.25;对兔耳皮肤全层损伤后不同时间点检测白细胞计数结果统计分析,第20天、第30天试验组的白细胞计数低于对照组;HE染色提示试验组毛细血管密度更高;试验组和对照组VEGF的阳性表达率分别为71.43%和35.71%,差异均具有统计学意义(P<0.05)。结论低能量半导体激光照射治疗,可通过降低白细胞计数、促进创面血管新生及上调VEGF的表达而有效缩短兔耳皮肤全层损伤的愈合时间、减轻创面挛缩程度。

Objective To explore the repairing effect and mechanism of 650 nm low energy semiconductor laser on full-thickness skin injury in rabbit ear.Methods A 2 cm×2 cm full-thickness skin injury model was established in SPF rabbit ears and then models were randomly divided into control group and experimental group.From the 11 th day afte modeling,the wounds in the control group were cleaned with normal saline every day,and experimental group were cleaned with normal saline and treated with 650 nm low energy semiconductor laser.The wound healing time,contrac-ture index,white blood cell count,histomorphological changes and the expression of vascular endothelial growth factor(VEGF)were detected.Results The average healing time in the experimental group and the control group were 23.79±3.75 days and 26.68±4.35 days respectively,the contracture indexes were 0.09±0.43 and 0.22±0.25 respectively.White blood cell count in experimental group was significantly lower than the control group at the 20 th and 30 th day.HE staining indicated higher capillary density in experimental group,compared with the control group(35.71%),the positive expression rate of VEGF in experimental group were 71.43%(P<0.05).Conclusion Low energy semiconductor laser irradiation can shorten the healing time effectively and reduce the degree of wound contracture of full-thickness skin injury in rabbit ear by decreasing white blood cell count,promoting wound angiogenesis and up-regulating the expression of VEGF.