摘要
目的 :明确异常瘢痕成纤维细胞的凋亡特性及激素治疗瘢痕的机理。方法 :以瘢痕疙瘩、增生性瘢痕和正常皮肤 (各 6例 )为材料 ,在体外对低血清和氟美松对不同成纤维细胞的细胞凋亡及与凋亡有关的蛋白Bax和Bcl-2的表达的影响进行了研究 ;同时 ,对 6例增生性瘢痕局部注射康宁克通后 3d和 7d的细胞凋亡和相关基因c-myc的表达进行了在体研究。结果 :在低血清中发生细胞凋亡正常皮肤成纤维细胞多于增生性瘢痕 ,增生性瘢痕多于瘢痕疙瘩 ,同时伴有Bax/Bcl-2蛋白比值的改变 ;氟美松能诱导三者成纤维细胞凋亡 ,尤其是增生性瘢痕的成纤维细胞 ;康宁克通能引起c -myc基因表达增高导致细胞凋亡。 结论 :不同成纤维细胞特性存在差异 ;
Objective:This study was carried out to determine the apoptosis character of fibroblasts from abnormal scars and mechanism of cortisone on abnormal scars.Methods:6 samples of keloid,hypertrophic scar and normal skin were collected respectively.The effects of media containing low serum or dexamethasone on apoptosis and expressions of apoptosis relative proteinsBax and Bcl2 of different fibroblasts were studied in vitro; At the same time,6 samples of hypertrophic scars from 6 patients were investigated in vivo,and apoptosis and expression of cmyc gene were detected on the 3 rd day and 7 th day after intralesional injection of kenalog.Results:(1)In media containing low serum,apoptosis of fibroblasts from normal skin takes place more seriously than that from hypertrophic scar,and apoptosis of fibroblasts from hypertrophic scar takes place more seriously than that from keloid as well in correspondence with changes of radios of Bax/Bcl2 proteins.(2)Dexamethasone can induce apoptosis of different fibroblasts especially fibroblasts from hypertrophic scar in correspondence with increasing of Bax/Bcl2 radio.(3)Kenalog can induce higher expression of cmyc gene leading apoptosis in hypertrophic scars in vivo.Conclusion:The characters of fibroblasts from keloid,hypertrophic scar and normal skin,and apoptosis induced by cortisone is one of mechanisms why cortisone can alleviate abnormal scars.
出处
《杭州医学高等专科学校学报》
2000年第1期6-10,共5页
Journal of Hangzhou Medical College