“紫草素”是有效治疗银屑病的传统中药紫草的提取物，其作用靶点和机制一直是我们研究的焦点。前期实验中我们发现，IL-17刺激HaCaT细胞的过度增殖可被紫草素抑制。应用PCR Array技术定位出用药前后差异性表达的基因——CCAAT增强子结合蛋白δ（CEBPD）在银屑病动物模型及患者组织标本中的表达明显减少。并且，将紫草素配制成紫草素油外用于银屑病小鼠模型皮损处可对皮损有良好的治疗作用。据此我们得到两个提示：1）CEBPD在银屑病的发生、发展中扮演较重要角色。2）CEBPD可能是紫草素抑制角质形成细胞过度增殖的作用靶点。在后续研究中我们拟通过临床组织观察、蛋白表型检测、信号通路调控探索、转基因鼠体内实验佐证等一系列研究，部分阐明CEBPD在角质形成细胞过度增殖和银屑病发病中所扮演的角色及紫草素的干预机制。为临床上中药治疗银屑病等皮肤病或自身免疫性疾病提供更可靠的理论及实验依据。

Shikonin is one of the main components of lithospermum erythrorhizon which traditional medicine could treat psoriasis effectively. The target and development have always been the focus of our research. In a previous study, we found that CCAAT/enhancer-binding proteins-δ(CEBPD) is a critical factor by PCR Array. It’s down-expressed in psoriatic epidermis both in human and psoriasis-like mice model. Meanwhile, in the vivo, we found that shikonin oil could cure the psoriatic lesion of mouse. On the strength of previous study, we hypothesize that CEBPD would be a significant target in the development of keratinocytes proliferate and shikonin would cure psoriasis by means of CEBPD. In this study, we will figure out the role of CEBPD in psoriasis’s treatment by shikonin from a series of experiments. For instance the clinical observation、cell molecular research、the study of signal transduction pathways regulation mechanism and establish an psoriasis-like mice model by CEBPD knocked out. In vitro and vivo to explored the regulation mechanism of CEBPD in the keratinocytes via MAPK pathway and the intervention of shikonin. This project may be extremely valuable to define a novel target for the treatment of psoriasis.