PI3K/AKT/mTOR通路
蛋白激酶B
地塞米松
传统医学
红景天苷
医学
药理学
化学
内分泌学
信号转导
生物化学
作者
Y.J. Lee,Jeongjin Park,Woojin Jun
标识
DOI:10.1089/jmf.2025.k.0050
摘要
Turcz. water extract (PUW) in mice subjected to dexamethasone-induced muscle atrophy. Mice exhibiting dexamethasone-induced muscle atrophy experienced weight loss, reduced muscle mass, and functional decline. However, PUW administration effectively reversed these effects by maintaining muscle mass and strength, decreasing protein degradation-related marker expression, and enhancing signaling for protein synthesis. Notably, phosphorylations of mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase beta-1, and eukaryotic translation initiation factor 4E-binding protein 1 were significantly enhanced in the PUW group, indicating the activation of anabolic signaling. Overall, PUW alleviates muscle atrophy induced by dexamethasone by modulating the balance between protein degradation and synthesis through regulation of the ubiquitin-proteasome system and phosphoinositide 3-kinase/protein kinase B/mTOR pathway. These findings reveal the potential of PUW as a natural therapeutic agent for preventing or managing muscle wasting.
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