CAJ | 학술논문

目的：观察重组人内抑素( rhEndostatin)对兔耳瘢痕增生的抑制作用,探讨其部分作用机制。方法建立兔耳增生性瘢痕(HS)模型,瘢痕块内局部注射 rhEndostatin (1．25、2．5、5 g/L),观察瘢痕大体形态及组织学变化,免疫组织化学检测瘢痕组织Ⅰ、Ⅲ型胶原表达,电镜观察瘢痕组织成纤维细胞凋亡。结果与模型组和生理盐水组比较,2．5 g/L和5 g/L rhEndostatin组瘢痕平坦,面积减小,质地变软,瘢痕增生指数降低( P<0．05)；微血管密度降低( P<0．05)；Ⅰ、Ⅲ型胶原表达水平降低( P<0．05)；成纤维细胞凋亡。结论rhEndostatin 可抑制 HS 形成,该作用可能与 rhEndostatin抑制血管生成,进而促进增生性瘢痕成纤维细胞( HSFs)凋亡,减少胶原的产生与沉积有关。
목적：관찰중조인내억소( rhEndostatin)대토이반흔증생적억제작용,탐토기부분작용궤제。방법건립토이증생성반흔(HS)모형,반흔괴내국부주사 rhEndostatin (1．25、2．5、5 g/L),관찰반흔대체형태급조직학변화,면역조직화학검측반흔조직Ⅰ、Ⅲ형효원표체,전경관찰반흔조직성섬유세포조망。결과여모형조화생리염수조비교,2．5 g/L화5 g/L rhEndostatin조반흔평탄,면적감소,질지변연,반흔증생지수강저( P<0．05)；미혈관밀도강저( P<0．05)；Ⅰ、Ⅲ형효원표체수평강저( P<0．05)；성섬유세포조망。결론rhEndostatin 가억제 HS 형성,해작용가능여 rhEndostatin억제혈관생성,진이촉진증생성반흔성섬유세포( HSFs)조망,감소효원적산생여침적유관。
Objective To investigate the therapeutic effects of recombinant human endostatin ( rhEndostatin ) on hypertrophic scar ( HS ) and explore the possible mechanism of action involved. Methods A rabbit ear model with hypertrophic scars was established. Recombinant human endostatin injections were applied to the scars of the experimental group topically in different concentrations (1. 25, 2. 5, 5 g/L). The changes of macroscopic charac-teristics of scars were examined. Light microscopy and transmission electron microscopy were used for histomorpho-metric analysis. The levels of collagens Ⅰ and Ⅲ were detected by immunohistochemistry. Results Compared with physiological saline group and model group, group treated with rhEndostatin 2. 5 g/L and 5. 0 g/L showed sig-nificant reduction in height, volume and hardness, it resulted in a statistically significant reduction in the scar ele-vation index, the microvessel density and the expression of type Ⅰ and Ⅲ collagens (P<0. 05). An observation under transmission electron microscopy revealed that some fibroblasts nucleus ruptured and disintegrated and apop-totic body were observed in rhEndostatin 5 g/L group, but seldom found in triamcinolone group. Conclusion The findings of this study suggest that rhEndostatin has a markedly inhibitive effect on the formation of hypertrophic scar. It suppresses angiogenesis, and subsequently promotes HSFs apoptosis and reduces the overproduction and excessive deposition of collagen may account for this result.