银屑病中药复方制剂01（PSORI-CM01）介导的微小RNA-31对角蛋白6的抑制作用：一种改善银屑病的新方法
MicroRNA-31 mediated inhibition of keratin 6 by PSORI-CM01: a novel approach to psoriasis amelioration.
作者信息
Wang Shilei, Wang Jingkai, Pan Helin, Yang Ruogu, Zeng Fanli, Fang Yongfei, Zhang Jinwei
机构信息
Chongqing Hospital of Traditional Chinese Medicine, Chongqing University of Traditional Chinese Medicine, Chongqing, China.
Chongqing General Hospital, Chongqing University, Chongqing, China.
出版信息
Front Chem. 2025 Jul 18;13:1636529. doi: 10.3389/fchem.2025.1636529. eCollection 2025.
BACKGROUND
Psoriasis vulgaris is a serious noncommunicable disease, with no clear cause or cure. Expression of microRNA-31 (miR-31) is significantly increased in the cutaneous tissue of psoriasis vulgaris patients. Keratin 6 (Krt6) serves as a pivotal biomarker in the diagnostic and therapeutic approaches for psoriasis vulgaris. PSORI-CM01, a traditional Chinese medicine formulation comprising seven medicinal herbs, is employed in China for the therapeutic management of psoriasis vulgaris. However, its anti-psoriatic mechanism warrants further investigations. In this study, the underlying anti-psoriasis mechanism of PSORI-CM01dependent of miR-31 and Krt6 was explored.
METHODS
, BALB/c mice were subjected to treatment with imiquimod (IMQ) to establish a psoriasis-like murine model. These psoriasis-like mice were then administered varying concentrations of PSORI-CM01. Following this, evaluations were performed on their Psoriasis Area and Severity Index (PASI) scores, epidermal thickness, and the expression levels of miR-31 and Krt6. HaCaT cells were subjected to treatment with interleukin-6 (IL-6) to create a psoriasis-like cellular model. Following this, the psoriasis-like keratinocytes were administered varying concentrations of PSORI-CM01, and the expression levels of miR-31 were quantified. In addition, these psoriasis-like keratinocytes were transfected with miR-31 mimics and subsequently treated with PSORI-CM01. The expression levels of Krt6 were then quantified and subjected to analysis.
RESULTS
, PSORI-CM01 significantly alleviated the clinical-like manifestations of erythema, scales, and thickening in psoriasis-like mice, and it also reduced the PASI scores; Different concentrations of PSORI-CM01 significantly decreased epidermal thickness and the expression of miR-31 and Krt6 in psoriasis-like mice in a dose-dependent manner. , PSORI-CM01 significantly inhibited the expression of miR-31 and Krt6 in psoriasis-like keratinocytes; However, the decreased Krt6 protein expression was restored by miR-31 mimics.
CONCLUSION
PSORI-CM01 may improve psoriasis-like lesions by inhibiting expression of Krt6 protein dependent of miR-31.
背景
寻常型银屑病是一种严重的非传染性疾病，病因不明且无法治愈。寻常型银屑病患者皮肤组织中微小RNA-31（miR-31）的表达显著增加。角蛋白6（Krt6）是寻常型银屑病诊断和治疗方法中的关键生物标志物。PSORI-CM01是一种由七种草药组成的中药配方，在中国用于寻常型银屑病的治疗管理。然而，其抗银屑病机制有待进一步研究。在本研究中，探讨了PSORI-CM01依赖miR-31和Krt6的潜在抗银屑病机制。
方法
将BALB/c小鼠用咪喹莫特（IMQ）处理以建立银屑病样小鼠模型。然后给这些银屑病样小鼠施用不同浓度的PSORI-CM01。在此之后，对它们的银屑病面积和严重程度指数（PASI）评分、表皮厚度以及miR-31和Krt6的表达水平进行评估。用人白细胞介素-6（IL-6）处理HaCaT细胞以建立银屑病样细胞模型。在此之后，给这些银屑病样角质形成细胞施用不同浓度的PSORI-CM01，并对miR-31的表达水平进行定量。此外，用miR-31模拟物转染这些银屑病样角质形成细胞，随后用PSORI-CM01处理。然后对Krt6的表达水平进行定量并进行分析。
结果
PSORI-CM01显著减轻了银屑病样小鼠的红斑、鳞屑和增厚等临床样表现，并且还降低了PASI评分；不同浓度的PSORI-CM01以剂量依赖的方式显著降低了银屑病样小鼠的表皮厚度以及miR-31和Krt6的表达。PSORI-CM01显著抑制了银屑病样角质形成细胞中miR-31和Krt6的表达；然而，miR-31模拟物恢复了Krt6蛋白表达的降低。
结论
PSORI-CM01可能通过抑制依赖miR-31的Krt6蛋白表达来改善银屑病样病变。
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