颌面部皮肤瘢痕严重影响患者的面部外形和功能。成纤维细胞是皮肤创口愈合过程中胶原合成与瘢痕形成的主要“参与者”，更是瘢痕防治的关键靶细胞。近期文献报道：皮肤中CD26+成纤维细胞亚群主要负责创口愈合过程中的胶原合成与分泌。我们前期研究发现：miR-29b能转录后抑制HSP47/Col 1的表达，减少胶原合成，抑制瘢痕形成；miR-29b-金纳米复合物能将miR-29b高效转运至成纤维细胞内并发挥生物学效应。本课题基于生物靶向治疗策略，拟在细胞、分子和动物水平上采用抗体片段制备、透射电镜、激光共聚焦和流式分选等技术构建靶向CD26+成纤维细胞亚群的anti-CD26Fab-miR-29b-金纳米复合物并验证其抑制胶原合成减轻瘢痕形成的效能，旨在探索anti-CD26Fab-miR-29b-金纳米复合物靶向CD26+成纤维细胞抑制瘢痕形成的可行性及有效性，为研发皮肤瘢痕防治新策略奠定前期基础。

Facial scar significantly impairs the facial morphology and functions of patients. Fibroblast plays a pivotal role in collagen synthesis and scar formation during skin wound healing, and remains the key target for anti-scar therapeutic manipulation. Recent literature has uncovered that the CD26+fibroblast subpopulation is the primary cell type responsible for collagen biosynthesis and secretion during skin wound repair. Our previous studies have revealed that miR-29b can reduce collagen biosynthesis and scar formation during skin wound healing via post-transcriptional inhibition of HSP47 and Col 1α1 expression. AuNP-miR-29b complex delivery can transfer miR-29b efficiently into fibroblast and in turn exert its biological functions. In the present study, based on the rationale of biological target therapy, we attempt to design and construct the anti-CD26Fab-miR-29b-AuNP complex with antibody fragment production, TEM (transmission electron microscope), LSCM (laser scanning confocal microscope) and FACS (fluorescence-based cell sorting) and perform a series of in vitro and in vivo experiments at the cellular, molecular and animal levels to deliver the miR-29b into CD26+ fibroblast and testify the feasibility and efficiency of this nanocomposite complex therapy to reduce scar formation. This novel nanocomposite-based anti-scar strategy might offer scientific proof-of principle evidence to support the targeted therapeutic strategy against skin scar.