目的探讨4-羟苯基维胺脂(N4-hydroxyphenyl retinode,4-HPR)联合超声治疗对免耳增生性瘢痕组织成纤维细胞凋亡与Bax蛋白表达的影响。方法建立兔耳增生性瘢痕模型,分别设立对照组、4-HPR组、超声组、4-HPR+超声组,兔耳瘢痕形成后进行4-HPR注射及超声治疗,采用免疫组化的方法观察真皮层成纤维细胞中Bax蛋白的表达,对比研究在兔耳增生性瘢痕实验性治疗过程中4-HPR联舍超声治疗对成纤维细胞凋亡活性的影响。结果与对照组相比,兔耳增生性瘢痕组织在4-HPR和超声联合治疗时对成纤维细胞Bax蛋白的表达明显增加,差异有统计学意义(P〈0.05),并且具有4-HPR浓度依赖性和超声剂量强度依赖性。结论4-HPR联合超声治疗可能通过Bax途径促进增生性瘢痕组织真皮层的成纤维细胞凋亡,对兔耳增生性瘢痕有明显的防治作用。
Objective To investigate the effect of N-4-hydroxyphenyl retinode (4-HPR)combined ultrasound on apoptosis of rabbit ear hypertrophic scar fibroblasts and Bax protein expression. Methods Set up four groups ot to rabbit ear hypertrophic scar model, that is control group, 4-HPR group, ultrasonic radiation group and 4-HPR combine ultrasonic radiation group. After rabbit ear scar formation, we used 4-HPR injection and ultrasound treatment. We observed Bax protein expression in dermal fibrob/asts by immunohistochemica] method, comparative studied the effect of 4-HPR combined ultrasound therapy on apoptotic activity of fibroblasts during the experimental treatment process of rabbit ear hypertrophic scars. Results Compared with the control group, Bax protein expression of fibroblasts increased in the 4-HPR and ultrasound combined irradiation in the rabbit ear hypertrophic scar tissue, and the difference was statistically significant (P 〈 0. 05 ). And its role showed as 4-HPR concentration-dependent and ultrasonic radiation intensity dependent. Conclusion 4-HPR and ultrasonic irradiation promoted the apoptosis of fibroblast in dermal layer of hypertrophic scar tissue through the Bax pathway, which plays a role of prevention and treatment for the rabbit ear hypertrophic scar.