详细信息

Isoliquiritigenin, a Bioactive Blood Component Derived from Licorice, Activates Nrf2 Enzymes to Confer Protection Against Radiation-Induced Nerve Injury  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:Isoliquiritigenin, a Bioactive Blood Component Derived from Licorice, Activates Nrf2 Enzymes to Confer Protection Against Radiation-Induced Nerve Injury

作者:Yao, Juan[1,2];Ma, Jiaqi[1,2];Lin, Huanhuan[1,2];Shao, Changxin[1,2];Liu, Xuefeng[1,2];Jin, Xiaojie[1,2]

第一作者:姚娟;Yao, Juan

通信作者:Yao, J[1];Jin, XJ[1];Yao, J[2];Jin, XJ[2]

机构:[1]Gansu Univ Chinese Med, Coll Pharm, Lanzhou 730000, Peoples R China;[2]Gansu Phammaceut Ind Innovat Res Inst, Lanzhou 730000, Peoples R China

第一机构:甘肃中医药大学药学院(西北中藏药协同创新中心办公室)

通信机构:[1]corresponding author), Gansu Univ Chinese Med, Coll Pharm, Lanzhou 730000, Peoples R China;[2]corresponding author), Gansu Phammaceut Ind Innovat Res Inst, Lanzhou 730000, Peoples R China.|[1073501e14fb35863569f]甘肃中医药大学药学院(西北中藏药协同创新中心办公室);[10735]甘肃中医药大学;

年份:2026

卷号:15

期号:5

外文期刊名:ANTIOXIDANTS

收录:;Scopus(收录号:2-s2.0-105040260903);WOS:【SCI-EXPANDED(收录号:WOS:001774066900001)】;

基金:This work was supported by the Gansu Longyuan Youth Talent Innovation and Entrepreneurship Project (No. 2022LQGR56), National Natural Science Foundation of China (No. 82104370), and Gansu Provincial Natural Science Foundation (No. 21JR1RA270).

语种:英文

外文关键词:isoliquiritigenin; Nrf2; Keap1; radiation; oxidative stress

摘要:Licorice is a traditional Chinese medicine; however, its bioactive constituents and specific molecular mechanisms responsible for protecting against radiation-induced brain injury remain poorly elucidated. Oxidative stress overactivation acts as the core pathological mechanism underlying radiation-triggered neuronal injury. This study aimed to investigate the neuroprotective effect and underlying mechanism of isoliquiritigenin (ISL), a major blood-absorbed component of licorice, against radiation-induced neural injury in C57BL/6J mice via the Keap1-Nrf2 signaling pathway. Molecular docking and MST analysis verified the strong binding affinity of ISL to Keap1. In vitro, ISL restored the viability of X-ray-irradiated PC12 cells; reduced LDH release and intracellular ROS accumulation; and enhanced SOD1 activity, GSH content, and T-AOC levels. Moreover, ISL upregulated the expression of antioxidant-related genes and induced Nrf2 nuclear translocation. In vivo, oral ISL administration ameliorated radiation-induced cognitive impairment, improved spatial learning and memory, alleviated hippocampal neuronal loss, and increased cerebral cortical Nrf2 expression in C57BL/6J mice. In conclusion, ISL alleviates radiation-induced neuronal injury by suppressing oxidative stress and activating the Keap1-Nrf2 signaling pathway, thus representing a promising therapeutic agent for the prevention and treatment of radiation brain injury.

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