相关实验视频

Updated: Jun 23, 2025

Immunometabolic Circuits in Infection for Advancing Host Directed Therapies

Immunometabolic Circuits in Infection for Advancing Host Directed Therapies

Published on: September 13, 2024

康迪塞调节微质M2极化与线粒体代谢重编程相结合,通过准HKII和PDK2来调节

Xin Zhong¹, Shiqiang Gong^1,2, Linghui Meng³

¹School of Pharmacy, China Medical University, Shenyang, Liaoning, 110122, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|June 18, 2024

概括

在阿尔茨海默病模型中,cordycepin通过重编程微质代谢来增强认知功能. 这促进了M2极化和神经元的生存,提供了一个新的治疗策略.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
代谢过程中的代谢.

背景情况:

微质 (MG) M1/M2极化在阿尔茨海默病 (AD) 病原和认知功能中至关重要.
代谢重编程在微质极化中的作用及其在阿尔茨海默病中的机制仍然不清楚.

研究的目的:

在AD小鼠模型中研究cordycepin对微质极化和代谢重编程的影响.
阐明基底的分子机制,通过它cordycepin发挥其抗老年痴呆的作用.

主要方法:

向APP/PS1小鼠注射cordycepin以评估认知功能和神经元损伤.
微质M1/M2极化和代谢途径 (OXPHOS,糖解) 的分析.
高性能液体染色学-并联质谱学 (HPLC-MS/MS) 来确认 mitochondria 中的 cordycepin 分布.
作为潜在的标,对六酶II (HKII) 和酸盐脱酶激酶2 (PDK2) 的研究.

主要成果:

科迪塞宾在APP/PS1小鼠中改善了认知功能和记忆,减少了神经元损伤.
科迪塞宾诱导了MG-M2极化和代谢重编程,增加了氧化酸化 (OXPHOS) 和糖解.
科迪塞宾缓解了微质中的线粒体损伤,并促进了M2极化.
确定了HKII和PDK2作为潜在的目标;cordycepin对这些调节的糖解和OXPHOS的作用,驱动M2极化.

结论:

康迪塞通过重编程微质代谢和促进M2极化来改善AD类病理,而不是直接保护神经元.
该机制涉及针对HKII和PDK2来分别增强糖解和OXPHOS,从而改善神经元存活率和抗老年症效应.

关键词:

香港II 香港II 香港II 在PDK2中使用PDK2.科尔迪cepin是什么意思代谢重编程是指代谢重编程.微质分极化微质分极化

更多相关视频

Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis

Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis

Published on: November 28, 2015

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility

Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility

Published on: April 13, 2017

相关概念视频

Electron Transport Chain: Complex I and II

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...

Calmodulin-dependent Signaling

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...