相关实验视频

Updated: Jul 12, 2025

Methods to Assess Subcellular Compartments of Muscle in C. elegans

Methods to Assess Subcellular Compartments of Muscle in C. elegans

Published on: November 13, 2014

L-Isoleucine可以逆转高氨血症引起的髓管线粒体功能障碍和线粒体衰老后的衰老

Avinash Kumar¹, Annette Bellar², Saurabh Mishra²

¹Department of Gastroenterology, Hepatology and Nutrition, All India Institute of Medical Sciences, New Delhi, India.

The Journal of nutritional biochemistry

|October 23, 2023

概括

L-Isoleucine (Ile) 逆转肌肉细胞中的氨毒性影响,恢复线粒体功能并减少衰老. 这种必不可少的氨基酸独立于LAT1载体对抗高氨血引起的损伤.

科学领域:

细胞的新陈代谢
线粒体生物学线粒体生物学
慢性疾病病理生理学慢性疾病病理生理学

背景情况:

由于慢性疾病中氨代谢障碍导致的超氨血,会损害骨肌肉功能.
氨的毒性导致阿尔法-甲酸盐的损失,线粒体功能障碍,以及与衰老相关的分子表型 (SAMP).
分支链氨基酸 (BCAAs),如L-Isoleucine (Ile),在细胞能量和变症中发挥作用.

研究的目的:

研究L-Isoleucine (Ile) 是否可以逆转高氨血症诱导的线粒体功能障碍和肌肉细胞中的SAMP.
探索BCAA载体LAT1/SLC7A5在Ile治疗效果中的作用.

主要方法:

利用差异化小鼠C2C12神经管 (早期和衰老通道) 和人类诱导的多能干细胞衍生的神经管 (hiPSCM).
暴露于高氨血的细胞和评估线粒体功能,ATP含量和蛋白质合成.
研究了Ile在具有和没有LAT1/SLC7A5载体表达的细胞中的影响.

主要成果:

L-Isoleucine (Ile) 恢复了超氨基菌管和hiPSCM中的最大呼吸能力和线粒体复合体I,II和III功能.
它逆转了高氨血症引起的ATP含量和全球蛋白质合成的减少.
它对蛋白质合成和逆衰老标记的关键调节者进行了正常化,独立于LAT1/SLC7A5转运体活性.

结论:

L-Isoleucine (Ile) 有效地逆转高氨血症诱导的线粒体氧化功能障碍和骨肌细胞中的SAMP.
伊莱的有益作用独立于LAT1/SLC7A5氨基酸载体.
它显示出作为治疗剂的潜力,可以减轻慢性疾病中的氨毒性.

关键词:

这是一种L-Isoleucine.这种疾病叫做阿纳普勒索斯.这种疾病叫做cataplerosis.过高氨血的情况.线粒体氧化过程中的线粒体氧化.这是一个myotube.

更多相关视频

Isolation and Differentiation of Primary Myoblasts from Mouse Skeletal Muscle Explants

Isolation and Differentiation of Primary Myoblasts from Mouse Skeletal Muscle Explants

Published on: October 15, 2019

Evaluation of Amino Acid Consumption in Cultured Bone Cells and Isolated Bone Shafts

Evaluation of Amino Acid Consumption in Cultured Bone Cells and Isolated Bone Shafts

Published on: April 13, 2022

相关概念视频

Mitochondria

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...