Abstract：
Psoriasis is one of the most prevalent and chronic inflammatory disease of the skin, associated with disrupted barrier function. Currently, a widely accepted, generally usable cell culture model has not been developed yet. In the present work, we aimed to establish a co-culture model with human keratinocyte (HaCaT) and human monocyte cells (THP-1) induced by Imiquimod (IMQ), which acts on the TLR7 receptor. The role of TLR7 expressed on THP-1 cells was confirmed by immunofluorescence staining of NF-κB activation. Chloroquine (CH) was used as a receptor inhibitor, in the presence or absence of which the NF-κB pathway was activated. We determined the most effective proliferation-stimulating IMQ concentration by RTCA method and the hyperproliferative effect was investigated by wound-healing test. The effect of IMQ was compared with the effects of the anthocyanin (AC) components from the anti-inflammatory sour cherry extract that we have already studied. We found that IMQ significantly increased the migration rate however, the combined treatment resulted in a decreased migration rate compared to the IMQ treatment alone. Inflammatory cytokines were measured from the supernatant of co-culture by ELISA. During the development of the co-culture intended to model psoriasis, we confirmed the induction effect of IMQ and in the case of AC treatment, we supported the stabilizing effect of the barrier.
摘要：
银屑病是皮肤最常见的慢性炎症性疾病之一,与屏障功能中断有关。目前,一个被广泛接受的,通常可用的细胞培养模型尚未开发。在目前的工作中,我们的目的是建立由咪喹莫特（IMQ）诱导的人角质形成细胞（HaCaT）和人单核细胞（THP-1）共培养模型，它作用于TLR7受体。通过NF-κB活化的免疫荧光染色证实了THP-1细胞上表达的TLR7的作用。氯喹（CH）被用作受体抑制剂，在存在或不存在的情况下，NF-κB途径被激活。我们通过RTCA方法确定了最有效的刺激增殖的IMQ浓度，并通过伤口愈合试验研究了过度增殖作用。将IMQ的作用与我们已经研究的抗炎酸樱桃提取物中花青素(AC)成分的作用进行比较。我们发现IMQ显着提高了迁移率，与单独的IMQ治疗相比,联合治疗导致迁移率降低.通过ELISA从共培养的上清液测量炎性细胞因子。在开发用于银屑病模型的共培养过程中，我们证实了IMQ的诱导作用，在AC治疗的情况下，我们支持屏障的稳定作用。
