摘要
目的探讨人端粒酶逆转录酶（human telomerase revere transcriptase,hTERT）、bcl-2蛋白在病理性瘢痕组织中的表达及其在瘢痕发生、发展中的作用和意义。方法采用链霉亲和素-过氧化物酶免疫组织化学法,对18例瘢痕疙瘩组织、18例增生性瘢痕和18例正常皮肤标本中成纤维细胞hTERT和bcl-2蛋白表达进行检测,用SPSS统计软件进行相应统计学分析。结果hTERT和bcl-2蛋白在瘢痕疙瘩组织中有较强的表达,阳性表达率分别为72.2%和83.3%。在增生性瘢痕和正常皮肤组织中表达较弱,前者显著高于后两者,其差异具有统计学意义（P〈0.01）。增生性瘢痕hTERT的表达高于正常皮肤组织,其差异有统计学意义（P〈0.05）,但bcl-2表达两者差异无统计学意义（P〉0.05）。hTERT蛋白和bcl-2蛋白在病理性瘢痕组织中的表达呈显著正相关（P〈0.01）。结论端粒酶和bcl-2与病理性瘢痕的发生、发展及其演变过程密切相关,两者可能存在某种相互调控机制。设想减少hTERT和bcl-2在病理性瘢痕成纤维细胞的过度表达或许是抑制瘢痕增生的新途径。
Objective To study the expression of hTERT and bcl-2 in the abnormal scars and its role and significance in the formation and development of abnormal scars. Methods The expression of hTERT and bcl-2 was observed in hypertrophic scars （18 cases）, keloids （18 cases） and normal skins （18 cases） with SP immunohistochemical method. The data were analyzed by statistical software （SPSS）. Resuits The expression of human telomerase reverse transcriptase （hTERT） and bcl-2 protein was strong in keloids （72.2 %, 83.3 % ） while they were weak in hypertrophic scars and normal skin. The expression levels of hTERT and bcl-2 in the fibroblasts of keloids were significantly higher than in both hypertrophic scars and normal skin （ P〈0. 01）;There were significant difference between human normal skin and hypertrophic scar fibroblasts in hTERT expression （ P〈0.05）, but no significant difference in bcl-2 expression （P〉0.05）. The expression of hTERT protein in the abnormal scars had significant correlation with the expression of bcl-2 （P〈0.01）. Conclusions Over expression of hTERT and bcl-2 may be related to the pathogensis of the abnormal scars, and there may be some regulatory mechanisms between hTERT and bcl-2 gene. The telomerase and bcl-2 appear to have close relation to the formation and development of abnormal scars, To find a way to decrease the expression level of hTERT and bcl-2 in fibroblasts may be a new approach to inhibit abnormal scar hypertrophy.
出处
《中华医学美学美容杂志》
2007年第3期137-140,共4页
Chinese Journal of Medical Aesthetics and Cosmetology
