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葛根素通过抑制TNF-α/NF-κB信号通路延缓地塞米松诱导的小鼠肌肉减少症的肌肉萎缩进展

Puerarin Delays the Progression of Muscle Atrophy in Mice With Dexamethasone-Induced Sarcopenia Through Inhibiting the TNF-α/NF-κB Pathway.

作者信息

Lin Shangjin, Cheng Ying, Chen Xiuxiu, Yang Fengjian, Fan Yongqian, Yang Shengwu

机构信息

Department of Orthopedics The First Affiliated Hospital of Wenzhou Medical University Wenzhou China.

Shanghai Key Laboratory of Clinical Geriatric Medicine Shanghai China.

出版信息

Food Sci Nutr. 2025 Apr 18;13(4):e70166. doi: 10.1002/fsn3.70166. eCollection 2025 Apr.

Abstract

Sarcopenia, marked by the loss of muscle mass and function, is a chronic condition that worsens with age. Currently, there are no effective drugs for its treatment. Puerarin, a potent natural compound extracted from the root of , exhibits various pharmacological properties, including anti-inflammatory, antioxidative, and anti-apoptotic effects. It remains unclear whether puerarin possesses anti-muscle atrophy capabilities. This study aims to evaluate the effectiveness of puerarin in delaying the development of muscle atrophy in mice with dexamethasone-induced sarcopenia and to explore the underlying molecular mechanisms. Experimental findings reveal that puerarin effectively alleviates a range of physiological and behavioral changes caused by dexamethasone, including weight loss, deterioration in muscle mass and function, and destruction of the ultrastructure of muscle fibers. Notably, puerarin significantly enhances muscle mass and function in mice with dexamethasone-induced sarcopenia, reduces the release of pro-inflammatory cytokines while promoting the production of anti-inflammatory factors, lowers oxidative stress, inhibits the expression of muscle apoptosis proteins, and decelerates muscle atrophy development by suppressing the TNF-α/NF-κB signaling pathway. In conclusion, these findings not only further confirm the potential value of puerarin as a therapeutic drug for sarcopenia but also provide new directions and theoretical foundations for future research.

摘要

肌肉减少症以肌肉质量和功能丧失为特征,是一种随年龄增长而恶化的慢性疾病。目前,尚无有效的治疗药物。葛根素是从葛根中提取的一种有效的天然化合物,具有多种药理特性,包括抗炎、抗氧化和抗凋亡作用。葛根素是否具有抗肌肉萎缩能力尚不清楚。本研究旨在评估葛根素在延缓地塞米松诱导的肌肉减少症小鼠肌肉萎缩发展方面的有效性,并探讨其潜在的分子机制。实验结果表明,葛根素能有效缓解地塞米松引起的一系列生理和行为变化,包括体重减轻、肌肉质量和功能恶化以及肌肉纤维超微结构破坏。值得注意的是,葛根素显著提高了地塞米松诱导的肌肉减少症小鼠的肌肉质量和功能,减少促炎细胞因子的释放,同时促进抗炎因子的产生,降低氧化应激,抑制肌肉凋亡蛋白的表达,并通过抑制TNF-α/NF-κB信号通路减缓肌肉萎缩的发展。总之,这些发现不仅进一步证实了葛根素作为治疗肌肉减少症药物的潜在价值,也为未来的研究提供了新的方向和理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a69/12006924/48c7beecc031/FSN3-13-e70166-g003.jpg

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