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当归芍药散通过调节AMPK/Nrf2/NF-κB信号通路缓解MAFLD

Danggui Shaoyao Powder Alleviates MAFLD by Regulating the AMPK/Nrf2/NF-κB Signaling Pathway.

科研进展PubMed 论文(TCM 食品)机译
  • 期刊Combinatorial chemistry & high throughput screening(Comb Chem High Throughput Screen)
  • 发表时间2026-10-08
  • 作者Biao Y, Chu X, Gao X, Zhang D, Gu Y, Wang Y, Zhang Y
  • DOI10.2174/0113862073477943260930051022
  • PMID42872447

摘要机译

[引言]本研究旨在探讨当归芍药散(DSP)治疗代谢性dysfunction-associated性脂肪肝(MAFLD)的机制。[方法]通过喂养高脂饲料(HFD)建立MAFLD大鼠。造模12周后,DSP治疗与造模4周同时给药。

评估的参数包括脂代谢、肝功能、氧化应激、炎症因子和活性氧(ROS)水平。还评估了肝脏组织病理学变化。使用Western blot分析与AMP活化蛋白激酶(AMPK)/核因子红细胞2相关因子2(Nrf2)/核因子-κB(NF-κB)信号通路相关的蛋白质。

此外,AMPK激活剂和AMPK和Nrf2抑制剂证实了AMPK/Nrf2/NF-κB信号通路参与棕榈酸(PA)诱导的HepG2细胞。[结果]结果表明,DSP有效调节MAFLD大鼠脂质代谢,改善肝功能,减少氧化损伤和炎症。

在PA处理的HepG2细胞中,DSP显著降低脂质积累、氧化应激和炎症。此外,DSP增加AMPK磷酸化,导致Nrf2激活和抑制MAFLD大鼠和HepG2细胞中的NF-κB磷酸化。[结论]结果表明,DSP减轻与MAFLD相关的氧化损伤和炎症,可能是通过调节AMPK/Nrf2/NF-κB信号通路。

展开英文摘要原文

【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.

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