评估咪喹莫特诱导的银屑病模型中作为银屑病标记物的 Kynu、Defb2、Camp 和 Penk 表达水平

IF 4.4 3区 医学 Q2 CELL BIOLOGY Mediators of Inflammation Pub Date : 2024-07-16 eCollection Date: 2024-01-01 DOI:10.1155/2024/5821996
Zahra Emami, Saeideh Sadat Shobeiri, Razia Khorrami, Navideh Haghnavaz, Mohammad Ali Rezaee, Malihe Moghadam, Safoora Pordel, Mojtaba Sankian
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引用次数: 0

摘要

背景:银屑病是一种非传染性自身炎症性慢性皮肤病。迄今为止,一些炎症基因在银屑病小鼠模型中被上调。本研究检测了在咪喹莫特诱导的银屑病小鼠模型中,L-犬尿素酶(Kynu)、cathelicidin抗菌肽(Camp)、β-防御素2(Defb2)和proenkephalin(Penk)的皮肤mRNA表达变化:C57BL/6雌性小鼠分为三组。两组小鼠背侧皮肤均涂抹咪喹莫特(IMQ)乳膏以诱导银屑病炎症。治疗组在含 M7 抗 IL-17A aptamer 的水凝胶治疗 10 分钟后使用 IMQ。阴性对照组使用凡士林(Vas)。根据银屑病面积严重程度指数(PASI)评分、组织病理学以及使用实时 PCR 的 Kynu、Camp、Defb2 和 Penk 的 mRNA 表达水平对银屑病皮损进行评估。为了评估全身反应,还评估了脾脏和淋巴结指数:结果:IMQ 组的 PASI 和表皮厚度评分分别为 6.01 分和 1.96 分,服用合剂后分别显著降至 1.15 分和 0.90 分(P < 0.05)。IMQ组的脾脏和淋巴结指数有所上升,但在使用合酶后略有下降(P > 0.05)。此外,与 Vas 小鼠相比,IMQ 处理区 Kynu、Defb2、Camp 和 Penk 基因的 mRNA 表达水平分别显著增加了 2.70、4.56、3.29 和 2.61 倍(P < 0.05)。而合剂处理区域的这些基因表达水平则明显下降(P < 0.05)。Kynu、Penk和Camp的表达水平与红斑呈正相关,Camp的表达与PASI、鳞屑和厚度呈正相关(P < 0.05):根据我们的研究结果,Kynu、Camp和Penk似乎可被视为评估IMQ诱导的银屑病的适当标记物。此外,抗IL-17适配体还能在该小鼠模型中下调这些重要基因。
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Evaluation of Kynu, Defb2, Camp, and Penk Expression Levels as Psoriasis Marker in the Imiquimod-Induced Psoriasis Model.

Background: 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.

Materials and methods: 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.

Results: 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).

Conclusion: 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.

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来源期刊
Mediators of Inflammation
Mediators of Inflammation 医学-免疫学
CiteScore
8.70
自引率
0.00%
发文量
202
审稿时长
4 months
期刊介绍: Mediators of Inflammation is a peer-reviewed, Open Access journal that publishes original research and review articles on all types of inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, leukotrienes, PAF, biological response modifiers and the family of cell adhesion-promoting molecules.
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