药理学
酒精性肝病
代谢组学
信号转导
免疫印迹
污渍
作用机理
肝损伤
类黄酮
代谢途径
化学
医学
花生四烯酸
生物化学
肝病
酒
氧化应激
根(腹足类)
毒性
生物
药效学
作者
Jiale Zhang,Miaoyu Ren,Mengran Qi,Fangyu Cui,Yangmiao Sun,Y Z Zhang,Xuanfeng YUE
标识
DOI:10.1142/s0192415x26500345
摘要
ALD models, and assessed the extent of pathological damage using Hematoxylin-Eosin (HE) staining. The relevant assay kits were used to measure inflammatory responses and oxidative stress-related indicators. In addition, a combination of metabolomics and network pharmacology was used to elucidate the PI3K/AKT signaling pathway as a potential mechanism of FRP-based ALD treatment. Western blotting experiments were conducted to measure the expression levels of key proteins, and the pharmacodynamic results showed that FRP reduced liver injury. Metabolomics revealed that FRP significantly regulated the levels of 73 metabolites involving the glycerophospholipid metabolism, arachidonic acid metabolism, and alpha-linolenic acid metabolism pathways. Network pharmacology results suggested that INS, AKT1, and TNF may be potential targets, and Western blot experiments showed that FRP could alleviate ALD by activating the PI3K/AKT pathway. These results indicated that FRP could exert its therapeutic effect against ALD by regulating the PI3K/AKT signaling pathway, and establish a robust application foundation for further research.
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