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PSORI-CM02 的抗血管生成疗效及其在银屑病和 中的相关机制。

Anti-Angiogenic Efficacy of PSORI-CM02 and the Associated Mechanism in Psoriasis and .

机构信息

The Second Clinical Medical College, Guangzhou University of Chinese Medicine, Guangzhou, China.

State Key Laboratory of Dampness Syndrome of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, China.

出版信息

Front Immunol. 2021 Apr 30;12:649591. doi: 10.3389/fimmu.2021.649591. eCollection 2021.

DOI:10.3389/fimmu.2021.649591
PMID:33995368
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8119787/
Abstract

Psoriasis is a chronic proliferative autoimmune dermatologic disease characterised by abnormal angiogenesis. Thus, regulating angiogenesis in the skin is an important treatment strategy for psoriasis. PSORI-CM02, an empirical Chinese medicine formula optimised from Yin Xie Ling, was created by the Chinese medicine specialist, Guo-Wei Xuan. Clinical studies have shown that PSORI-CM02 is safe and effective for the treatment of psoriasis. However, its anti-psoriatic mechanisms remain to be further explored. In this study, we investigated the effects of PSORI-CM02 on angiogenesis in the skin and the underlying mechanisms in IL-17A-stimulated human umbilical vein endothelial cells (HUVECs) and a murine model of imiquimod (IMQ)-induced psoriasis. , PSORI-CM02 significantly inhibited the proliferation and migration of IL-17A-stimulated HUVECs in a dose-dependent manner. Further, it markedly regulated the antioxidative/oxidative status and inflammation; suppressed the expression of VEGF, VEGFR1, VEGFR2, ANG1, and HIF-1α; and reduced the phosphorylation of MAPK signalling pathway components in IL-17A-stimulated HUVECs. studies showed that PSORI-CM02 markedly reduced angiogenesis in the skin of mice with IMQ-induced psoriasis, while significantly rebalancing antioxidant/oxidant levels; inhibiting the production of IL-6, TNF-α, IL-17A, and IL-17F; and repressing the synthesis of angiogenic mediators. In addition, PSORI-CM02 markedly reduced the activation of the MAPK signalling pathway in psoriatic skin tissue. Taken together, our results demonstrated that PSORI-CM02 inhibited psoriatic angiogenesis by reducing the oxidative status and inflammation, suppressing the expression of angiogenesis-related molecules, and inhibiting the activation of the MAPK signalling pathway and .

摘要

银屑病是一种慢性增生性自身免疫性皮肤病,其特征为异常血管生成。因此,调节皮肤中的血管生成是治疗银屑病的重要策略。PSORI-CM02 是一种经验性的中药配方,由中医专家郭维勋从银屑灵优化而来。临床研究表明,PSORI-CM02 治疗银屑病安全有效。然而,其抗银屑病的机制仍有待进一步探索。在这项研究中,我们研究了 PSORI-CM02 对白细胞介素-17A 刺激的人脐静脉内皮细胞(HUVEC)和咪喹莫特(IMQ)诱导的银屑病小鼠模型中血管生成的影响及其潜在机制。结果表明,PSORI-CM02 可显著抑制白细胞介素-17A 刺激的 HUVEC 的增殖和迁移,呈剂量依赖性。此外,它还可显著调节氧化应激/抗氧化状态和炎症;抑制 VEGF、VEGFR1、VEGFR2、ANG1 和 HIF-1α的表达;并减少白细胞介素-17A 刺激的 HUVEC 中 MAPK 信号通路成分的磷酸化。体内研究表明,PSORI-CM02 可显著减少咪喹莫特诱导的银屑病小鼠皮肤中的血管生成,同时显著重新平衡抗氧化/氧化水平;抑制 IL-6、TNF-α、IL-17A 和 IL-17F 的产生;并抑制血管生成介质的合成。此外,PSORI-CM02 还可显著降低银屑病皮肤组织中 MAPK 信号通路的激活。综上所述,我们的研究结果表明,PSORI-CM02 通过降低氧化应激和炎症水平、抑制血管生成相关分子的表达以及抑制 MAPK 信号通路的激活来抑制银屑病的血管生成。

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Oxidative Stress as an Important Contributor to the Pathogenesis of Psoriasis.氧化应激是银屑病发病机制的重要因素。
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SB218078 inhibits angiogenesis and epithelial-mesenchymal transition in breast cancer.SB218078抑制乳腺癌中的血管生成和上皮-间质转化。
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