叶黄素与矢车菊素-3-0-葡萄糖苷联合使用对小鼠肝氧化损伤的改善机制

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中图分类号：TS201.2 文献标识码：A 文章编号： 1000-4440（2025）11-2242-15

Abstract：To analyze themechanismof actionof lutein（LUT）and cyanidin-3-O-glucoside（C3G）alone and in combination on liver oxidativedamage，this studyconstructed a mouse liver oxidative damage model induced bycarbon tetrachloride（ CCl4 ），and compared the effects of LUT， C3G and LC（LUT + C3G）treatments on liver oxidative markers，Nrf2 pathway regulatory gene expression levels and gut microbiota structure in mice.The results showed that compared with CC 4 treatment，LUT，C3G and LCtreatmentsincreased theactivitiesoftotalsuperoxidedismutase（T-SOD）andcatalase（CAT），elevatedglutathione （GSH）contentandtotalantioxidantcapacity（T-AOC）intheliverof mice，andefectivelyinhibitedtheproductionof malondialdehyde（MDA），therebyaleviating hepaticoxidative damage inmice.ComparedwiththeLUT-treated group，the GSH content and T-AOC in the liver of LC-treated mice increased by 50.66% and 39.23% ，respectively，and the MDA content decreased by 404% . Compared with CCl4 treatment，LUT，C3G and LC treatments could increase the expression levelsof Nrf2 ，NQ01 and HO -1 genes and decrease the expression level of Keapl gene. The relative expression levels of Nrf2 ，NQO1 and HO I genes in LC treatment were 57.40% ， 46.50% and 42.77% higher than those in LUT treatment， while the relative expression level of Keapl gene was down-regulated by 40.88% . LUT， C3G and LC treatments significantly increasedthe productionof short-chain fattyacids（SCFA）andtherelativeabundanceof RikenellaceaeandAkkermansia bacteria，whileantibioticpretreatmentcould interferewiththeregulationofLUTandC3Gongutmicrobiotaandreducethe relativeabundanceofLachnospiraceaeandBacteroidaceaebacteria.In summary，thecombineduseofLUTand C3G can enhancetheactivtyofantioxidantenzymes inthe liver of mice，regulate the expression levelsof Nrf2 pathwayregulatory genes and improve the gut microbiota structure of mice.

Key words：lutein；cyanidin-3-O-glucoside； liver damage；antioxidant capacity；combination effe

动物肝脏具有代谢、解毒、转化、合成、免疫防御等多种重要生理功能[1]，氧化应激是肝损伤发生和持续的重要原因[2-3]。（剩余24036字）