中文摘要：

目的探讨分泌型凋亡相关蛋白1（secretedapoptosis-relatedprotein1，SARP1）调控增生性瘢痕患者的成纤维细胞（fibroblast，FB）凋亡的作用。方法构建SARP1腺病毒载体（Ad-sARPl）．感染瘢痕患者的皮肤FB，促进其表达SARP1蛋白，观察其蛋白表达后人FB增殖与凋亡的变化，明确SARP1蛋白对FB的调控作用，并通过转移酶介导的三磷酸脱氧鸟苷-生物素刻痕末端标记（TuNEL）方法、流式细胞仪（FACs）分析细胞增殖与凋亡动态变化。结果成功构建Ad-SARP1，并能够感染人FB，通过逆转录一聚合酶链式反应（RT-PCR）检测到SARP1的mRNA值明显增加，Western印迹方法检测SARP1蛋白表达明显增多（P〈0．05）；其蛋白表达后四甲基偶氮噻唑蓝（MTT）法检测，与带荧光的腺病毒空载体（Ad-EGFP）及对照组相比，Ad-SARP1感染的FB增殖活力均显著增高；TUNEL检测Ad-SARP1感染FB前后细胞凋亡结果显示，细胞凋亡明显受到抑制，凋亡阳性细胞变少，接近瘢痕成纤维细胞（HSFB）凋亡；FACS分析表明，感染组FB的细胞凋亡指数与对照组相比明显下降（P〈0．01）。结论sARP1参与调控增生性瘢痕患者的FB功能，抑制细胞凋亡，促进细胞增殖加快。

英文摘要：

Objective To explore the effects of secreted apoptosis-related protein 1 （SARP1） on apoptosis of the hyperstrophic scar fibroblasts （HSFB） and its regulating mechnisms. Methods The recombinant vector was identified by enzyme digestion analysis. And the virus supernatant of the re- combinant vector was extracted from packaged 293 cells, then it infected the skin fibroblasts from hy- pertrophic scar patients, which aimed to promote its expression of SARP1 protein. After adenovirus infection, the expression of SARP1 in the {ibroblasts was confirmed by RT-PCR and Western Blot. The effect of SARP1 on proliferation of HSFB was detected by MTT assay, and the effect of SARP1 on apoptosis of HSFB was detected and change of the cells functions were analyzed by FACS. Results Recombinants were confirmed. After adenovirus infection, both protein and mRNA of SARP1 were detected in HSFB. And the mRNA value of SARPlwas detected to increase significantly by RT-PCR and the protein expression was detected to increase significantly by Western blot （P~0.05）. The pro- liferation in the groups of the adenovirus infection and HSFB was positively regulated by SARP1 （P% 0.01） and the apoptosis of them was inhibited by the expression of SARP1 as compared to the control groups of HSFB and Ad-EGFP. It showed that the apoptosis index decreased as compared the group of infected fibroblasts to the control group by flow cytometry. Conclusions SARP1 could be highly expressed in HSFB by adenovirus infection, exhibiting the proliferation-enhancing and apoptosis-inhib- iting effects on HSFB.