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

葛根素通过抑制 TNF-α/NF-β 通路延缓地塞米松诱导的肌肉减少症小鼠的肌肉萎缩进程

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作者:Lin Shangjin, Cheng Ying, Chen Xiuxiu, Yang Fengjian, Fan Yongqian, Yang Shengwu
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 Pueraria lobata, 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.

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