相关实验视频

Updated: Jul 17, 2025

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness

Published on: March 18, 2022

在骨关节炎中,FGF1通过调节AMPK/Nrf2通路来减少软骨损伤

Yun-Xuan Li¹, Jun Shu¹, Nan-Nan Kou¹

¹Department of Traumatology, The Second Affiliated Hospital of Kunming Medical University, 374 Dianmian Avenue, Wuhua District, Kunming, 650000, Yunnan, China.

Journal of molecular histology

|September 2, 2023

概括

纤维细胞生长因子1 (FGF1) 降低通过激活AMPK和Nrf2通路,显示出对骨关节炎 (OA) 的保护作用. 这项研究揭示了FGF1的存在.

科学领域:

生物化学生物化学
分子生物学分子生物学
整形外科整形外科整形外科

背景情况:

骨关节炎 (OA) 是一种由细胞因子和生长因子影响的退行性关节疾病.
纤维细胞生长因子1 (FGF1) 在OA病变发生中的作用需要进一步阐明.
氧化应激和特定的分子通路与OA软骨破坏有关.

研究的目的:

研究纤维细胞生长因子1 (FGF1) 对骨关节炎的保护作用.
阐明FGF1参与OA的潜在分子机制.
在OA模型中评估FGF1调节的体内疗效.

主要方法:

试验室研究涉及FGF1在冠状细胞中的淘汰.
在体内评估使用中介阴囊 (DMM) 和前/后十字带截面模型的不稳定.
对蛋白质表达 (Nrf2,HO-1) 和酸化 (AMPK) 的分析.
针对Nrf2和AMPK的淘汰实验,以评估它们的作用.

主要成果:

在骨关节炎模型中,FGF1倒置逆转了氧化损伤.
抑制FGF1增加了Nrf2和HO-1的蛋白质表达,与AMPK酸化有关.
Nrf2的淘汰消除了FGF1的抗氧化作用的淘汰.
在OA中,AMPK淘汰消除了FGF1淘汰的保护作用.

结论:

FGF1的淘汰证明了对骨关节炎的显著保护作用.
这种机制涉及到关节性红细胞中AMPK和Nrf2通路的激活.
针对FGF1提供了一个潜在的治疗策略,用于预防和逆转OA.

关键词:

Amp-激活的蛋白质激酶激酶是什么纤维细胞生长因子1 核因子红色素2相关因子2的核因子骨关节炎是一种骨关节炎.

更多相关视频

Creation of a Knee Joint-on-a-Chip for Modeling Joint Diseases and Testing Drugs

Creation of a Knee Joint-on-a-Chip for Modeling Joint Diseases and Testing Drugs

Published on: January 27, 2023

A Reproducible Cartilage Impact Model to Generate Post-Traumatic Osteoarthritis in the Rabbit

A Reproducible Cartilage Impact Model to Generate Post-Traumatic Osteoarthritis in the Rabbit

Published on: November 21, 2023

相关概念视频

NF-κB-dependent Signaling Pathway

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...

TGF - β Signaling Pathway

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...

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...

GPCRs Regulate Adenylyl Cylase Activity

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...