瘢痕是烧伤及创伤后常见的并发症, 寻找新型疗法迫在眉睫。Shikonin，紫草的有效成分，被证实诱导肿瘤细胞凋亡, 但是否诱导瘢痕细胞凋亡仍未知。鉴于细胞凋亡在瘢痕组织重塑中的作用, 我们假设Shikonin诱导瘢痕成纤维细胞(HSF)凋亡而具修复增生性瘢痕的潜力。我们最近的研究发现Shikonin诱导HSF凋亡, 且对正常角质形成细胞没影响。根据以上发现, 我们将运用细胞共培养系, 人体皮肤瘢痕等效模型及猪增生性瘢痕模型继续验证Shikonin诱导HSF凋亡及在增生性瘢痕修复中的作用。此外，本课题将采用Western Blot，RT-PCR，信号通路阻断剂, RNA干扰等技术, 研究两条经典凋亡通路（TNF-R1/Fas，Bcl-2介导的凋亡通路）与Shikonin诱导HSF凋亡的关系。 阐明Shikonin诱导HSF凋亡的信号转导机制和作用靶点，对开发新的瘢痕药物具有重要意义。

Scarring is a significant medical burden; financially to the health care system and physically and psychologically for patients. While research effort has been directed at the development of improved approaches to remediate scars, currently available therapies are not satisfactory due to their undesirable side-effects, complex delivery routes, requirements for long-term use and/or expense. Therefore, a novel scar remediation therapy that is simple to use and has minimal side-effects and cost is of great importance for both clinicians and patients.Shikonin, an active component extracted from Zi Cao has been demonstrated to induce apoptosis in cancer cell lines. This is of interest since apoptosis is known to be an essential component of scar tissue remodelling. This has led us to hypothesise that perhaps Shikonin may induce apoptosis in hypertrophic scar-derived human skin fibroblasts and may therefore hold potential for scar remediation. Our recent studies have revealed that Shikonin does indeed induces apoptosis in human scar-derived fibroblasts. The overall goal of this project is to verify Shikonin induces apoptosis in cells in scars using sophisticated 2-D and 3-D in vitro cell culture approaches, and a large animal in vivo hypertrophic scar model， as well as the underlying mechanisms invoked in the process of apoptosis using Western Blot, RT-PCR,signaling pathway inhibitors and RNA interference. Completion of these studies will generate the critical information necessary to developed into cost- and therapeutically-effective novel scar therapies.