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Nintedanib ameliorates imiquimod-induced psoriasis in mice by inhibiting NF-κB and VEGFR2 signaling
International Immunopharmacology ( IF 5.6 ) Pub Date : 2021-09-20 , DOI: 10.1016/j.intimp.2021.108129
Xiaohe Li 1 , Buri Xi 1 , Yang Miao 2 , Xiaoyang Ma 1 , Jianwei Zhang 2 , Jingjing Gao 3 , Wenguo Wei 4 , Honggang Zhou 1 , Cheng Yang 1
Affiliation  

Psoriasis is a common chronic skin disorder characterized by keratinocyte hyperproliferation with altered differentiation accompanied by increased inflammation and angiogenesis. Nintedanib is a tyrosine kinase inhibitor that has anti-inflammatory, anti-angiogenesis, and anti-fibrotic effects. In this study, we explored the potential effects and mechanisms of nintedanib on psoriasis in vivo and in vitro. In vivo experiments showed that nintedanib effectively alleviated imiquimod-induced psoriasis-like skin lesions and reduced psoriasis severity index scores. For the mechanism research, we mainly focused on the abnormal phenotype of keratinocyte in the pathogenesis of psoriasis. We used HaCaT cells in the in vitro experiments and the result revealed that nintedanib restored keratinocyte homeostasis by downregulated the expression of proinflammatory factors, inhibited hyperproliferation, promoted apoptosis, maintained normal differentiation via regulating the NF-κB pathway. In addition, nintedanib regulated angiogenesis by inhibiting VEGFR2 activity. In summary, our study indicated that nintedanib is a promising candidate medication for psoriatic treatment.



中文翻译:

尼达尼布通过抑制 NF-κB 和 VEGFR2 信号传导改善咪喹莫特诱导的小鼠银屑病

银屑病是一种常见的慢性皮肤病,其特征是角质形成细胞过度增殖,分化改变,炎症和血管生成增加。尼达尼布是一种酪氨酸激酶抑制剂,具有抗炎、抗血管生成和抗纤维化作用。在本研究中,我们探讨了尼达尼布对体内银屑病的潜在影响和机制和体外。体内实验表明,尼达尼布可有效缓解咪喹莫特诱导的银屑病样皮肤损伤,并降低银屑病严重程度指数评分。对于机制研究,我们主要关注角化细胞异常表型在银屑病发病机制中的作用。我们在体外实验中使用了 HaCaT 细胞,结果表明尼达尼布通过下调促炎因子的表达来恢复角质形成细胞的稳态,抑制过度增殖,促进细胞凋亡,通过调节 NF-κB 通路维持正常分化。此外,尼达尼布通过抑制 VEGFR2 活性来调节血管生成。总之,我们的研究表明,尼达尼布是一种很有前途的银屑病治疗候选药物。

更新日期:2021-09-20
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