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用帕佐帕尼布准JNK1/2和P38基因激活蛋白激酶减轻了白色素诱导的肺纤维化

Rasha Abdelhady^1,2, Rabab H Sayed^3,4, Nancy S Younis^5,6

¹Department of Pharmacology and Toxicology, Faculty of Pharmacy, Fayoum University, Fayoum, Egypt.

Archiv der Pharmazie

|September 29, 2025

概括

帕佐帕尼布通过减少炎症和改善肺组织,在治疗肺纤维化方面表现有前途. 这项研究发现它抑制了与纤维化有关的关键蛋白质,为异常性肺纤维化提供了潜在的新疗法.

科学领域:

肺部医学肺部医学
药理学药理学是指药理学的学科.
分子生物学分子生物学

背景情况:

异形性肺纤维化 (IPF) 是一种常见的,渐进的间歇性肺病.
目前IPF的治疗疗法有效性有限,需要新的治疗策略.

研究的目的:

在小鼠模型中研究帕佐帕尼布在减轻白血素诱导的肺纤维化中的治疗潜力.
阐明帕佐帕尼布抗纤维作用背后的分子机制.

主要方法:

雄性小鼠被分为对照组,白素诱导的纤维化,和pazopanib治疗的小组.
肺纤维化被诱导使用白素,其次是pazopanib的管理.
分析了关键纤维化标记物,细胞因子和信号通路的基因和蛋白质表达水平.

主要成果:

帕佐帕尼布治疗显著改善了体重,并改善了肺纤维化组织病理特征.
帕佐帕尼布抑制了基因激活蛋白激酶激酶激酶2 (MEKK2) 和MEKK3的mRNA表达,降低了下游的p-JNK1/2和p-P38.
帕佐帕尼布使促炎性细胞因子 (IL-1β,IL-13,IL-33,TNF-α,NF-κB P65) 的水平正常化,并逆转了TGF-β1和α-SMA的增加.

结论:

帕佐帕尼布在白胺诱导的肺纤维化中显示出显著的抗纤维作用.
该机制涉及抑制MEKK2/MEKK3和调节JNK/P38信号通路.
帕佐帕尼布具有作为肺纤维化治疗药物的潜力.

关键词:

在JNK1/2中使用.在P3838中,它是P38的.布莱莫辛 (Bleomycin) 是一种可怕的药物.这就是巴索帕尼比巴巴巴巴巴巴巴.肺部纤维化肺部纤维化

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