Combinatorial chemistry & high throughput screening · 2026
Danggui Shaoyao Powder Alleviates MAFLD by Regulating the AMPK/Nrf2/NF-κB Signaling Pathway.
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Biao Yaning, Chu Xinqiao, Gao Xingxing, Zhang Dou, Gu Ying, Wang Yafen, Zhang Yixin
Аннотация
INTRODUCTION: This study aimed to investigate the mechanisms by which Danggui Shaoyao powder (DSP) treats metabolic dysfunction-associated fatty liver disease (MAFLD).
METHODS: The MAFLD rats were established by feeding a high-fat diet (HFD). After 12 weeks of modeling, DSP treatment was administered simultaneously with the modeling for 4 weeks. Parameters assessed included lipid metabolism, liver function, oxidative stress, inflammatory factors, and reactive oxygen species (ROS) levels. Hepatic histopathological changes were also evaluated. Proteins associated with the AMP-activated protein kinase (AMPK)/nuclear factor erythroid 2-related factor 2 (Nrf2)/nuclear factor-κB (NF-κB) signaling pathway were analyzed using western blot. Additionally, the involvement of the AMPK/Nrf2/NF-κB signaling pathway in palmitic acid (PA)-induced HepG2 cells was confirmed using an AMPK activator and AMPK and Nrf2 inhibitors.
RESULTS: Findings demonstrated that DSP effectively regulated lipid metabolism, improved liver function, and reduced oxidative injury and inflammation in MAFLD rats. In PA-treated HepG2 cells, DSP significantly decreased lipid accumulation, oxidative stress, and inflammation. Furthermore, DSP increased AMPK phosphorylation, leading to Nrf2 activation and inhibition of NF-κB phosphorylation in both MAFLD rats and HepG2 cells.
CONCLUSION: The results indicate that DSP mitigates oxidative damage and inflammation associated with MAFLD, likely by modulating the AMPK/Nrf2/NF-κB signaling pathway.
METHODS: The MAFLD rats were established by feeding a high-fat diet (HFD). After 12 weeks of modeling, DSP treatment was administered simultaneously with the modeling for 4 weeks. Parameters assessed included lipid metabolism, liver function, oxidative stress, inflammatory factors, and reactive oxygen species (ROS) levels. Hepatic histopathological changes were also evaluated. Proteins associated with the AMP-activated protein kinase (AMPK)/nuclear factor erythroid 2-related factor 2 (Nrf2)/nuclear factor-κB (NF-κB) signaling pathway were analyzed using western blot. Additionally, the involvement of the AMPK/Nrf2/NF-κB signaling pathway in palmitic acid (PA)-induced HepG2 cells was confirmed using an AMPK activator and AMPK and Nrf2 inhibitors.
RESULTS: Findings demonstrated that DSP effectively regulated lipid metabolism, improved liver function, and reduced oxidative injury and inflammation in MAFLD rats. In PA-treated HepG2 cells, DSP significantly decreased lipid accumulation, oxidative stress, and inflammation. Furthermore, DSP increased AMPK phosphorylation, leading to Nrf2 activation and inhibition of NF-κB phosphorylation in both MAFLD rats and HepG2 cells.
CONCLUSION: The results indicate that DSP mitigates oxidative damage and inflammation associated with MAFLD, likely by modulating the AMPK/Nrf2/NF-κB signaling pathway.