PDF(Pubmed)
Abstract：
UNASSIGNED: Psoriasis is a noncontagious auto-inflammatory chronic skin disease. So far, some of the inflammatory genes were upregulated in mouse model of psoriasis. This study examined changes in skin mRNA expression of L-kynureninase (Kynu), cathelicidin antimicrobial peptide (Camp), beta-defensin 2 (Defb2), and proenkephalin (Penk) in a mouse model of imiquimod-induced psoriasis.
UNASSIGNED: Tree groups of C57BL/6 female mice were allocated. The imiquimod (IMQ) cream was administered to the mice dorsal skin of the two groups to induce psoriatic inflammation. In the treatment group, IMQ was administered 10 min after hydrogel-containing M7 anti-IL-17A aptamer treatment. Vaseline (Vas) was administered to the negative control group. The psoriatic skin lesions were evaluated based on the psoriasis area severity index (PASI) score, histopathology, and mRNA expression levels of Kynu, Camp, Defb2, and Penk using real-time PCR. In order to assess the systemic response, the spleen and lymph node indexes were also evaluated.
UNASSIGNED: The PASI and epidermal thickness scores were 6.01 and 1.96, respectively, in the IMQ group, and they significantly decreased after aptamer administration to 1.15 and 0.90, respectively (P < 0.05). Spleen and lymph node indexes showed an increase in the IMQ group, followed by a slight decrease after aptamer treatment (P > 0.05). Additionally, the mRNA expression levels of Kynu, Defb2, Camp, and Penk genes in the IMQ-treated region showed a significant 2.70, 4.56, 3.29, and 2.61-fold increase relative to the Vas mice, respectively (P < 0.05). The aptamer-treated region exhibited a significant decrease in these gene expression levels (P < 0.05). A positive correlation was found between Kynu, Penk, and Camp expression levels and erythema, as well as Camp expression with PASI, scaling, and thickness (P < 0.05).
UNASSIGNED: According to our results, it seems that Kynu, Camp, and Penk can be considered appropriate markers for the evaluation of psoriasis in IMQ-induced psoriasis. Also, the anti-IL-17 aptamer downregulated these important genes in this mouse model.
UNASSIGNED: Tree groups of C57BL/6 female mice were allocated. The imiquimod (IMQ) cream was administered to the mice dorsal skin of the two groups to induce psoriatic inflammation. In the treatment group, IMQ was administered 10 min after hydrogel-containing M7 anti-IL-17A aptamer treatment. Vaseline (Vas) was administered to the negative control group. The psoriatic skin lesions were evaluated based on the psoriasis area severity index (PASI) score, histopathology, and mRNA expression levels of Kynu, Camp, Defb2, and Penk using real-time PCR. In order to assess the systemic response, the spleen and lymph node indexes were also evaluated.
UNASSIGNED: The PASI and epidermal thickness scores were 6.01 and 1.96, respectively, in the IMQ group, and they significantly decreased after aptamer administration to 1.15 and 0.90, respectively (P < 0.05). Spleen and lymph node indexes showed an increase in the IMQ group, followed by a slight decrease after aptamer treatment (P > 0.05). Additionally, the mRNA expression levels of Kynu, Defb2, Camp, and Penk genes in the IMQ-treated region showed a significant 2.70, 4.56, 3.29, and 2.61-fold increase relative to the Vas mice, respectively (P < 0.05). The aptamer-treated region exhibited a significant decrease in these gene expression levels (P < 0.05). A positive correlation was found between Kynu, Penk, and Camp expression levels and erythema, as well as Camp expression with PASI, scaling, and thickness (P < 0.05).
UNASSIGNED: According to our results, it seems that Kynu, Camp, and Penk can be considered appropriate markers for the evaluation of psoriasis in IMQ-induced psoriasis. Also, the anti-IL-17 aptamer downregulated these important genes in this mouse model.
摘要：
银屑病是一种非传染性的自身炎症性慢性皮肤病。到目前为止,一些炎症基因在银屑病小鼠模型中上调。这项研究检查了L-犬尿氨酸酶（Kynu）皮肤mRNA表达的变化，cathelicidin抗菌肽（Camp），β-防御素2（Defb2），和前脑啡肽（Penk）在咪喹莫特诱导的牛皮癣小鼠模型中。
■分配C57BL/6雌性小鼠的树组。将咪喹莫特（IMQ）乳膏施用于两组小鼠的背侧皮肤以诱导银屑病炎症。在治疗组中，在含有水凝胶的M7抗IL-17A适体治疗后10分钟施用IMQ。向阴性对照组施用凡士林(Vas)。根据银屑病面积严重程度指数(PASI)评分评估银屑病皮损,组织病理学,和Kynu的mRNA表达水平，营地,Defb2和Penk使用实时PCR。为了评估系统反应，还评估了脾脏和淋巴结指数。
■PASI和表皮厚度评分分别为6.01和1.96，在IMQ组中，适体给药后，它们分别显着降低至1.15和0.90（P<0.05）。脾脏和淋巴结指数显示IMQ组增加，适体处理后略有下降(P>0.05)。此外,Kynu的mRNA表达水平，Defb2坎普,IMQ处理区域中的Penk基因相对于Vas小鼠显示出显著的2.70、4.56、3.29和2.61倍的增加，分别为(P<0.05)。适体处理的区域表现出这些基因表达水平的显著降低(P<0.05)。Kynu之间呈正相关，Penk,和Camp表达水平和红斑，以及与PASI的Camp表达，缩放，厚度(P<0.05)。
■根据我们的结果，看来Kynu,营地,和Penk可以被认为是评估IMQ诱导的牛皮癣的合适标志物。此外，在这个小鼠模型中，抗IL-17适体下调了这些重要的基因。
■分配C57BL/6雌性小鼠的树组。将咪喹莫特（IMQ）乳膏施用于两组小鼠的背侧皮肤以诱导银屑病炎症。在治疗组中，在含有水凝胶的M7抗IL-17A适体治疗后10分钟施用IMQ。向阴性对照组施用凡士林(Vas)。根据银屑病面积严重程度指数(PASI)评分评估银屑病皮损,组织病理学,和Kynu的mRNA表达水平，营地,Defb2和Penk使用实时PCR。为了评估系统反应，还评估了脾脏和淋巴结指数。
■PASI和表皮厚度评分分别为6.01和1.96，在IMQ组中，适体给药后，它们分别显着降低至1.15和0.90（P<0.05）。脾脏和淋巴结指数显示IMQ组增加，适体处理后略有下降(P>0.05)。此外,Kynu的mRNA表达水平，Defb2坎普,IMQ处理区域中的Penk基因相对于Vas小鼠显示出显著的2.70、4.56、3.29和2.61倍的增加，分别为(P<0.05)。适体处理的区域表现出这些基因表达水平的显著降低(P<0.05)。Kynu之间呈正相关，Penk,和Camp表达水平和红斑，以及与PASI的Camp表达，缩放，厚度(P<0.05)。
■根据我们的结果，看来Kynu,营地,和Penk可以被认为是评估IMQ诱导的牛皮癣的合适标志物。此外，在这个小鼠模型中，抗IL-17适体下调了这些重要的基因。
