文献类型：期刊文献

英文题名：Alleviation Effect of the Secondary Metabolite of Anthocyanin (Protocatechuic Acid) on Heterocyclic Amine (IQ)-Induced Liver Injury and Its Underlying Mechanism

作者：Liu, Jiang[1,2];Zhao, Yanan[1,2];Chen, Leyao[1,2];Cao, Ran[1,2];Deng, Hongting[1,2];Teng, Hui[1,2];Chen, Lei[1,2]

机构：[1]Guangdong Ocean Univ, Key Lab Adv Proc Aquat Prod Guangdong Higher Educ, Guangdong Prov Engn Lab Marine Biol Prod, Guangdong Prov Key Lab Aquat Prod Proc & Safety,Gu, Zhanjiang 524088, Peoples R China;[2]Guangdong Ocean Univ, Shenzhen Inst, Shenzhen 518108, Peoples R China

年份：2025

外文期刊名：JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY

收录：SCI-EXPANDED(收录号：WOS:001461911000001)、、EI(收录号：20251518228597)、Scopus(收录号：2-s2.0-105003443728)、WOS

基金：This study was supported by the National Natural Science Foundation of China (Grant/Award Numbers: 32272315)

语种：英文

外文关键词：protocatechuic acid; 2-amino-3-methylimidazo[4,5-f] quinoline; intestinal barrier dysfunction; gut microbiota

外文摘要：Increased consumption of thermally processed meats caused a high risk of accumulation of heterocyclic amines (HCAs), which would lead to livery injuries and carcinogenic diseases in daily life. Our previous study found that cyanidin-3-glucoside expressed a protective effect on 2-amino-3-methylimidazo [4,5-f] quinoline (IQ)-induced liver injury, but its intrinsic mechanism in vivo was unclear. Thus, this study was aimed at investigating the alleviation effect of the secondary metabolite of anthocyanin (protocatechuic acid) on IQ-induced liver dysfunction and its underlying mechanism. The results demonstrated that 4 weeks of IQ (30 mg/kg) administration to C57BL/6 mice induced significant oxidative stress and liver injury, which were suppressed by PCA (10 and 20 mg/kg) supplement. Meanwhile, IQ-mediated liver inflammation was mitigated by PCA supplementation via suppressing NF-kappa B/MAPK pathways of signaling. Moreover, the PCA supplement significantly reversed IQ-induced intestinal damage and tight junction dysfunction. Concurrently, 16s rRNA sequencing data indicated by PCA reversed the IQ-disturbed SCFAs content and gut microbiota. Analysis of the correlation between intestinal damage and gut microbiota, with manufacturers of hepatic dysfunction, underscored the significance of the gut-liver axis in PCA-relieved liver injury stimulated via IQ. Taken together, PCA reduced IQ-induced liver damage via modifying the NF-kappa B/MAPK-NLRP3 inflammatory cascade, which was controlled by intestinal barrier failure mediated by the gut microbiota. In summary, our results offer new perspectives on microbiome-targeted therapeutic strategies for liver dysfunction associated with IQ.