文献类型：期刊文献

英文题名：Caffeic acid activates Nrf2 enzymes, providing protection against oxidative damage induced by ionizing radiation

作者：Yao, Juan[1];Liu, Yuanyuan[2];Lin, Huanhuan[1];Shao, Changxin[1];Jin, Xiaojie[1];Peng, Ting[1];Liu, Yongqi[2]

第一作者：姚娟

通信作者：Yao, J[1];Liu, YQ[2]

机构：[1]Gansu Univ Chinese Med, Coll Pharm, Lanzhou 730000, Peoples R China;[2]Gansu Univ Chinese Med, Coll Basic Med, 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 Univ Chinese Med, Coll Basic Med, Lanzhou 730000, Peoples R China.|[107351d2d02a88e1f325f]甘肃中医药大学基础医学院（敦煌医学研究所）;[10735]甘肃中医药大学;[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）;

年份：2025

卷号：224

外文期刊名：BRAIN RESEARCH BULLETIN

收录：;Scopus(收录号：2-s2.0-105001813779);WOS:【SCI-EXPANDED(收录号:WOS:001464407500001)】；

基金：The authors appreciate the financial support received from the Na-tional Natural Science Foundation of China (82104370) .

语种：英文

外文关键词：Caffeic acid; Ionizing radiation; Nrf2; Oxidative stress; Neuroprotection; Antioxidant

摘要：Caffeic acid (CA) is a prevalent polyphenolic compound commonly found in various plant-derived foods. Due to its diverse pharmacological properties, including antioxidant activity, cardiovascular protection, and immune regulation, CA has garnered significant attention. Ionizing radiation (IR) is extensively utilized across industrial sectors, agriculture, defense applications, scientific research, and clinical medicine; however, the detrimental effects of radiation on human health cannot be ignored. IR can directly damage the DNA, proteins, and lipids within macromolecules or ionize water molecules to generate substantial quantities of free radicals that indirectly harm cells, especially those in the brain which are highly susceptible to radiation exposure. Consequently, effective strategies for preventing and treating IR-induced neurological damage represent an urgent medical challenge that necessitates resolution. Our study aims to investigate the protective effects of CA against IRinduced neuronal cell damage along with elucidating its potential mechanisms of action. The results indicate that CA can covalently modify active cysteine residues on Keap1 protein altering its conformation; this modification disrupts the interaction between Keap1 and Nrf2 while facilitating Nrf2's translocation into the nucleus where it activates downstream expression of cellular protective factors such as heme oxygenase-1 (HO-1), NAD (P)H: quinone oxidoreductase 1 (NQO1), Thioredoxin Reductase-1 (TrxR1) and other cellular protective factors to play a role in countering radiation-induced neurological damage. In conclusion, CA emerges as an effective radioprotective agent capable of exerting antiradiation effects. Our findings provide valuable insights for developing novel therapeutic agents aimed at preventing and treating IR-induced neurological impairment.