银屑病是一种在遗传背景和环境因素共同作用下，由T细胞介导的以角质形成细胞过度增生、炎症细胞浸润和新生血管形成为主要特征的慢性炎症性皮肤病。异常活化的T 淋巴细胞及其过度产生的细胞因子是银屑病发病的中心环节，也是触发其病理改变的始动因素。T淋巴细胞的异常活化与浸润引起角质形成细胞过度增生、新生血管形成、血管通透性增加，从而表现出鳞屑、红斑、筛状出血等典型的银屑病临床症状。此病常反复发作，病程长、难以根治且大量脱屑，给患者的身心健康带来严重影响，是皮外科重点研究的疾病之一。中医认为“血热蕴毒、热毒入血伤络”是银屑病发病的主要病机之一，“凉血解毒”是其主要治则。本研究采用佛波醇酯（phorbol 12, 13-dibutyrate，PDB）和离子霉素（Ionomycin，Iono）刺激活化Jurkat T细胞株体外模拟银屑病的关键病理环节，采用血清药理学的方法，观察在凉血解毒治则指导下的治疗银屑病临床有效方剂凉血活血胶囊、其凉血、解毒组分以及本方中君药紫草的有效成分紫草素对T淋巴细胞增殖、活化、释放细胞因子及其信号转导通路的影响。研究采用CCK-8比色法、流式细胞术及酶联免疫吸附试验（enzyme linked immune sorbent assay，ELISA）分别观察凉血活血胶囊及其凉血、解毒组分含药血清对T细胞增殖、活化和释放细胞因子的影响。结果显示，高、中、低剂量的凉血活血胶囊全方含药血清及其凉血、解毒组分的含药血清均可显著降低活化的T淋巴细胞的活性，明显抑制细胞表面活化分子CD69的表达，并有效下调IFN-γ、IL-2和TNF-α的分泌。组间比较发现，全方组总体药效优于各拆方组，尤其在抑制细胞活性和降低TNF-α分泌上表现突出。解毒组除在调节IL-2和TNF-α分泌上作用与凉血组相当外，其余各项药效均优于凉血组；尤其是在对细胞活性及IFN-γ分泌的抑制作用方面，解毒组可接近全方的作用效果。紫草素对T淋巴细胞活化的作用结果显示，0.5~2µg/ml的紫草素均可显著抑制细胞活性、降低CD69的表达并可有效减少IFN-γ、IL-2和TNF-α的分泌。进一步研究其对信号转导通路的影响，采用流式细胞术发现紫草素可有效降低细胞内游离Ca2+浓度；ELISA法证实细胞内PKC磷酸化蛋白的含量明显降低；RT-PCR结果表明紫草素可明显抑制核转录因子NF-AT和AP-1组分c-Jun的mRNA表达；Western blot法也证明紫草素对c-Jun及NF-кB的蛋白表达具有一定的下调作用。以上各项指标均呈现出一定的量效关系。结论：凉血活血胶囊及其凉血、解毒组分均可抑制T淋巴细胞增殖、活化和释放细胞因子，且全方作用优于凉血、解毒拆方，提示银屑病血分“热”、“毒”并存，“血热蕴毒”是其重要病机，临床治疗凉血、解毒不可分割。具有凉血解毒作用的紫草素能通过对活化的T细胞信号转导通路的调控发挥免疫抑制作用。

Psoriasis is a chronic IFNlammatory skin disease characterized by T cell-mediated keratinocytes hyperproliferation, IFNlammatory cells IFNiltration and neovascularization on genetic and environmental backgrounds. Abnormally activated T lymphocytes and its excessive cytokines play central roles in the pathogenesis of psoriasis, which are the initiation of pathological alteration in psoriasis. The aberrant activation and IFNiltration of T lymphocytes induce the keratinocytes hyperproliferation, neovascularization and increased vascular permeability, which display the typical clinical symptom of silvery scales, erythema, and sieve-like bleeding. Psoriasis is a long-course and recurrent disease, and it is difficult to be cured. So it will impact the physical and mental health of patients. Psoriasis is one of the most important diseases in the dermatology surgery. The theory of Traditional Chinese Medicine (TCM) believes that the key pathogenesis of psoriasis is “heat accumulated in blood transforming into toxin, and then heat and toxin harm on collateral”. The main therapeutic is “cooling blood and detoxification”. In this study, Jurkat T cell lines are stimulated with phorbol 12, 13-dibutyrate(PDB) and Ionomycin(Iono) in vitro to simulate the key pathological aspects of psoriasis. Serum pharmacological method was used in the experiments. The effects of LingXueHuoXue capsule complete ingredients (LC) which is the clinical effective prescription for psoriasis under the guidance of therapeutic “cooling blood and detoxification”, its LiangXue(LX) and JieDu(JD) components, and shikonin from Lithospermum erythrorhizon which is the most important herb in LXHX capsule were studied on proliferation, activation, cytokine production and its possible signal transduction pathway of activated T lymphocytes.The CCK-8 assay was used for T cell proliferation, flow cytometry was adapted to CD69 expression, an early marker of T cell activation, and the level of cytokines was measured by enzyme linked immune sorbent assay (ELISA) in this study. The results showed that the drug serums both containing high, middle and low dosage of LC , and its LX and JD components all significantly inhibited the T lymphocyte activities. All groups of drug serum also obviously inhibited CD69 expression, decreased the level of IFN-γ，IL-2 and TNF-α. Among of the three groups, LC group was the superior, particularly on cells activities and TNF-α production. The inhibitions of JD group were stronger than LX group’s, except for the secretions of IL-2 and TNF-α. In addition, the immunosuppressions of JD group were close to the effects of LC especially on T cells activities and the level of IFN-γ.The results of shikonin on T lymphocytes activation showed that 0.5 to 2 µg/ml of shikonin significantly inhibited the cell activities, suppressed CD69 expression and decreased the level of IFN-γ、IL-2 and TNF-α. Further studies on the signal transduction pathway of T lymphocytes activation indicated that shikonin reduced the level of intracellular free calcium by flow cytometry, and decreased the phosphor-PKC content by ELISA. RT-PCR results deminstrated that all groups of shikonin distinctly inhibited mRNA expression of nuclear transcription factor NF-AT and c-jun, a subscription of AP-1. As well as, Western blot results displayed protein expression of c-Jun and NF-кB was downregulated by shikonin. All of the results above showed dose-dependents. Conclusion: LC and its LX and JD components can inhibit proliferation, activation and cytokine production of T lymphocytes, as well as, the effects of the complete prescription of LXHX is superior among the three groups. This suggests “heat and toxin coexist in blood” and “heat accumulated in blood transforming into toxin”, which is the key point of the pathogenic mechanisms in psoriasis, and cooling blood and detoxicification cannot be separated in clinical treatments. Shikonin, which has an effect on both cooling blood and detoxicification, can exert immunosuppression by regulating signal pathway of T lymphocytes activation.