相关实验视频

Updated: Jan 9, 2026

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Published on: May 3, 2024

在缺氧缺血性脑损伤中,ZFP36通过抑制TXNIP/NLRP3通路来减弱神经元亡和烧亡

Hengjiang Guo¹, Yan Jiang¹, Zhiqing Gu¹

¹Department of Anesthesiology, Shanghai Children's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200062, China.

|December 8, 2025

概括

手指蛋白36 (ZFP36) 通过减少神经炎症,防止缺氧缺血性脑损伤 (HIBD). 升级的ZFP36抑制TXNIP/NLRP3炎症酶通路,为HIBD提供了潜在的治疗策略.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
炎症研究炎症研究

背景情况:

缺氧缺血性脑损伤 (HIBD) 是新生儿死亡率和神经缺陷的主要原因.
神经炎症是HIBD中神经元损伤的关键因素.
指蛋白36 (ZFP36) 在HIBD中的作用尚不清楚.

研究的目的:

研究ZFP36在HIBD中的作用.
阐明ZFP36在HIBD中的作用的潜在分子机制.
评估ZFP36作为HIBD的潜在治疗点.

主要方法:

使用新生儿大鼠模型的HIBD和HT22海马神经元细胞经过氧气-葡萄糖剥夺/再氧化 (OGD/R).
使用腺相关病毒 (AAV) 和lentivirus用于ZFP36的淘汰和过度表达.
通过mRNA和蛋白质分析研究了ZFP36,铁素相互作用蛋白 (TXNIP) 和NLRP3炎症组之间的相互作用.

主要成果:

在HIBD模型中,ZFP36表达显著上调.
ZFP36中断加剧了HIBD和OGD/R诱导的神经元损伤,亡和烧亡.
ZFP36过度表达改善了HIBD和OGD/R诱导的神经元损伤.
ZFP36直接与TXNIP mRNA结合,促进其降解并抑制NLRP3炎症酶激活.

结论:

通过抑制神经炎症,ZFP36在HIBD中起着保护作用.
ZFP36通过抑制TXNIP/NLRP3炎症酶途径来发挥其保护作用.
ZFP36是缓解HIBD相关脑损伤的有希望的治疗标.

关键词:

缺氧性-缺血性脑损伤在NLRP3中,NLRP3是NLRP3中的一个.神经炎症是一种神经炎症.在TXNIP中,您可以使用TXNIP.ZFP36 ZFP36 是一个

更多相关视频

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells

Published on: October 20, 2022

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model

Published on: October 27, 2020

相关概念视频

The Extrinsic Apoptotic Pathway

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...

The Intrinsic Apoptotic Pathway

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

Apoptosis

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...