CAJ | 학술논문

目的：通过建立兔耳增生性瘢痕模型,研究肿瘤坏死因子α刺激基因-6( TSG-6)在增生性瘢痕形成过程中的作用及机制。方法建立兔耳增生性瘢痕模型,右侧耳创面为实验组,注射TSG-6,左侧均注射等量PBS作为对照组,通过比较各组瘢痕指数( SEI)及Ⅰ、Ⅲ型胶原表达的不同来评价瘢痕增生程度的差异。采用免疫组化法及逆转录聚合酶链反应( RT-PCR)法检测炎症因子白细胞介素-1β( IL-1β)、白细胞介素-6(IL-6)及肿瘤坏死因子-α(TNF-α)在各组中的表达；以透射电镜观察及TUNEL法检测瘢痕组织成纤维细胞凋亡的变化。结果与PBS对照组比较,TSG-6治疗组炎症因子IL-1β、IL-6及TNF-α表达减少炎症反应明显减轻,瘢痕组织成纤维细胞凋亡明显增多,且SEI及Ⅰ、Ⅲ型胶原含量均低于对照组,差异有统计学意义( P<0．05)。结论抗炎因子TSG-6能明显减弱增生性瘢痕的形成,其对瘢痕形成的抑制作用可能与抑制炎症反应及促进成纤维细胞凋亡相关。
목적：통과건립토이증생성반흔모형,연구종류배사인자α자격기인-6( TSG-6)재증생성반흔형성과정중적작용급궤제。방법건립토이증생성반흔모형,우측이창면위실험조,주사TSG-6,좌측균주사등량PBS작위대조조,통과비교각조반흔지수( SEI)급Ⅰ、Ⅲ형효원표체적불동래평개반흔증생정도적차이。채용면역조화법급역전록취합매련반응( RT-PCR)법검측염증인자백세포개소-1β( IL-1β)、백세포개소-6(IL-6)급종류배사인자-α(TNF-α)재각조중적표체；이투사전경관찰급TUNEL법검측반흔조직성섬유세포조망적변화。결과여PBS대조조비교,TSG-6치료조염증인자IL-1β、IL-6급TNF-α표체감소염증반응명현감경,반흔조직성섬유세포조망명현증다,차SEI급Ⅰ、Ⅲ형효원함량균저우대조조,차이유통계학의의( P<0．05)。결론항염인자TSG-6능명현감약증생성반흔적형성,기대반흔형성적억제작용가능여억제염증반응급촉진성섬유세포조망상관。
Objective To observe the effect of tumor necrosis factorαstimulated gene-6 ( TSG-6 ) on hypertrophic scarring by using a rabbit ear model. Methods TSG-6 and PBS were injected intradermally in the right and left ear wounds, respectively. Collagen I and III expression detected by immunohistochemistry and scar elevation index ( SEI) was used to evaluate the extent of scarring. The expression of inflammatory factors interleukin-1β( IL-1β) , interleukin-6 ( IL-6 ) and tumor necrosis factor-α( TNF-α) was detected by immunohistochemistry and reverse tran-scription polymerase chain reaction. Transmission electron microscope ( TEM) and TUNEL analyses were used to detect fibroblast apoptosis. Results Compared with control scars, TSG-6-treated wounds exhibited decreased in-flammation significantly as evidenced by the lower levels of IL-1β, IL-6 , TNF-α. The apoptosis rate was higher and the SEI and the synthesis of collagens I and III were significantly decreased in the TSG-6-treated scars ( P<0. 05 ) . Conclusion Immediate topical injection of TSG-6 during the wound healing process can reduce the severity of hy-pertrophic scarring in a rabbit model. The anti-cicatrix effect of TSG-6 may result from controlling inflammation, in-ducing fibroblast apoptosis and promoting collagen degradation.