Deng Dandan, Zhao Borong, Yang Hong, Wang Songsong, Geng Ziying, Zhou Jiangtao, Yang Guane, Han Liwen
School of Pharmaceutical Sciences, Shanxi Medical University, No. 56 South Xinjian Road, Taiyuan 030001, China.
School of Pharmaceutical Sciences & Institute of Materia Medica, Shandong First Medical University & Shandong Academy of Medical Science, No. 6699 Qingdao Road, Jinan 250117, China.
Pharmaceuticals (Basel). 2025 Jan 17;18(1):116. doi: 10.3390/ph18010116.
: Rhamnetin 3--α-rhamnoside (ARR) is a major flavonoid of the herb Franch. & Sav., which has been used for treating liver diseases in China. However, the protective effect of ARR on the liver has not been reported. : Zebrafish larvae were used as a visual animal model, and liver injury was induced by thioacetamide (TAA) for an acute liver injury (ALI) model. The hepatoprotective activity of ARR was evaluated by assessing liver morphology, liver function indices, oxidative stress, and the mRNA expression levels of inflammation-related genes in the zebrafish model. Additionally, the ROS level, inflammatory factors, and protein expression related to the IKKβ/NF-κB signaling pathway were measured to investigate a potential mechanism of ARR in HepG2 cells. : ARR ameliorated TAA-induced growth retardation, reduced liver injury phenotypes, and decreased oxidative stress in the zebrafish. ARR was also able to lower ROS levels in HepG2 cells, effectively inhibit the overactivation of the IKKβ/NF-κB signaling pathway in pathological conditions, inhibit NF-κB p65 translocation from the cytoplasm to the nucleus, and reduce the release of intracellular inflammatory factors. : ARR showed significant protective activity against TAA-induced liver injury in in vivo and in vitro models, and its potential mechanism was closely related to the IKKβ/NF-κB signaling pathway.
鼠李素3-α-鼠李糖苷(ARR)是鼠李科植物的一种主要黄酮类化合物,在中国已被用于治疗肝脏疾病。然而,ARR对肝脏的保护作用尚未见报道。
以斑马鱼幼体作为可视化动物模型,用硫代乙酰胺(TAA)诱导肝损伤建立急性肝损伤(ALI)模型。通过评估斑马鱼模型中的肝脏形态、肝功能指标、氧化应激以及炎症相关基因的mRNA表达水平,来评价ARR的肝保护活性。此外,检测了与IKKβ/NF-κB信号通路相关的活性氧水平、炎症因子和蛋白表达,以研究ARR在HepG2细胞中的潜在作用机制。
ARR改善了TAA诱导的斑马鱼生长迟缓,减轻了肝损伤表型,并降低了氧化应激。ARR还能够降低HepG2细胞中的活性氧水平,有效抑制病理条件下IKKβ/NF-κB信号通路的过度激活,抑制NF-κB p65从细胞质向细胞核的转位,并减少细胞内炎症因子的释放。
ARR在体内和体外模型中均显示出对TAA诱导的肝损伤具有显著的保护活性,其潜在机制与IKKβ/NF-κB信号通路密切相关。