相关实验视频

Updated: Jun 29, 2025

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis

Published on: May 9, 2025

佩菲西尼布通过阻断JAK3/STAT3通路的糖分解来缓解急性肺损伤

Wenyang Jiang¹, Jie Ren², Xiaochen Li³

¹Department of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan, China.

International immunopharmacology

|March 28, 2024

概括

佩菲西替尼是一种Janus激酶3 (JAK3) 抑制剂,通过阻断巨细胞糖解和热,有效降低急性肺损伤 (ALI). 这种保护作用依赖于JAK3,突出显示了ALI潜在的新治疗策略.

科学领域:

免疫学免疫学免疫学
药理学药理学是指药理学的学科.
肺部病理学肺部病理学

背景情况:

类风湿性关节炎的治疗包括像Peficitinib这样的JAK抑制剂.
大细胞糖解可以激活NLRP3炎症酶,导致热和急性肺损伤 (ALI).

研究的目的:

调查Peficitinib在减轻脂聚糖 (LPS) 诱导的ALI中的有效性.
确定佩菲西尼布是否抑制NLRP3炎症酶激活和相关途径.

主要方法:

在野生类型和JAK3淘汰赛小鼠中进行了peficitinib预处理,这些小鼠受到LPS的挑战.
对肺,炎症,亡和炎症酶激活的分析.
使用RAW264.7巨细胞进行体外研究,以评估Peficitinib对糖解和热的作用.

主要成果:

在小鼠中,peficitinib显著降低了LPS诱导的肺,炎症和亡.
佩菲西替尼 (peficitinib) 抑制了NLRP3炎症酶激活,糖解以及肺组织中的JAK3/STAT3信号传递.
在JAK3淘汰赛小鼠中缺乏保护作用,而JAK3过度表达在体外取消了Peficitinib的抑制作用.
由LPS诱导的JAK3/STAT3激活是由通类受体4 (TLR4) 介导的.

结论:

佩菲西尼布通过抑制巨细胞中JAK3介导的葡萄糖分解和热溶解来保护ALI.
通过TLR4激活的JAK3 / STAT3通路是Peficitinib对ALI的保护作用的关键目标.
佩菲西替尼 (peficitinib) 是一种治疗急性肺损伤的有前途的药物.

关键词:

急性肺损伤是什么?急性肺损伤是什么?葡萄糖溶解是什么? 葡萄糖溶解这就是JAK3的意义.巨细胞是一个巨细胞.佩菲西尼尼比 (Peficitinib) 是一种药物.

更多相关视频

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

Adoptive Transfer of IL-33-Stimulated Macrophages into Bleomycin-Induced Mouse Models to Study Their Effect on Idiopathic Pulmonary Fibrosis In Vivo

Adoptive Transfer of IL-33-Stimulated Macrophages into Bleomycin-Induced Mouse Models to Study Their Effect on Idiopathic Pulmonary Fibrosis In Vivo

Published on: May 5, 2023

相关概念视频

The JAK-STAT Signaling Pathway

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...