[1]陆风芹,李艳,李大婧,等.叶黄素与矢车菊素-3-O-葡萄糖苷联合使用对小鼠肝氧化损伤的改善机制[J].江苏农业学报,2025,(11):2242-2256.[doi:doi:10.3969/j.issn.1000-4440.2025.11.017]
 LU Fengqin,LI Yan,LI Dajing,et al.Ameliorative effect of lutein and cyanidin-3-O-glucoside on hepatic oxidative damage in mice[J].,2025,(11):2242-2256.[doi:doi:10.3969/j.issn.1000-4440.2025.11.017]
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叶黄素与矢车菊素-3-O-葡萄糖苷联合使用对小鼠肝氧化损伤的改善机制()

江苏农业学报[ISSN:1006-6977/CN:61-1281/TN]

卷:
期数:
2025年11期
页码:
2242-2256
栏目:
加工贮藏·质量安全
出版日期:
2025-11-30

文章信息/Info

Title:
Ameliorative effect of lutein and cyanidin-3-O-glucoside on hepatic oxidative damage in mice
作者:
陆风芹12李艳12李大婧12周存山1徐亚元12何伟伟12戴竹青12冯蕾12连运河3张钟元12
(1.江苏大学食品与生物工程学院,江苏镇江212013;2.江苏省农业科学院农产品加工研究所,江苏南京210014;3.晨光生物科技集团股份有限公司,河北石家庄050000)
Author(s):
LU Fengqin12LI Yan12LI Dajing12ZHOU Cunshan1XU Yayuan12HE Weiwei12DAI Zhuqing12FENG Lei12LIAN Yunhe3ZHANG Zhongyuan12
(1.School of Food and Biological Engineering, Jiangsu University, Zhenjiang 212013, China;2.Institute of Agricultural Products Processing, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, China;3.Chenguang Biotechnology Group Co., Ltd., Shijiazhuang 050000, China)
关键词:
叶黄素矢车菊素-3-O-葡萄糖苷肝脏损伤抗氧化能力协同效应
Keywords:
luteincyanidin-3-O-glucosideliver damageantioxidant capacitycombination effect
分类号:
TS201.2
DOI:
doi:10.3969/j.issn.1000-4440.2025.11.017
文献标志码:
A
摘要:
为解析叶黄素(Lutein,LUT)和矢车菊素-3-O-葡萄糖苷(Cyanidin-3-O-glucoside,C3G)单独及联合使用使肝脏免受氧化损伤的作用机制,本研究以四氯化碳(CCl4)诱导构建小鼠肝脏氧化损伤模型,比较LUT、C3G及LC(LUT+C3G)处理对小鼠肝脏氧化标志物、Nrf2通路调控基因表达水平及肠道菌群结构的影响。结果表明,与CCl4处理相比,LUT、C3G、LC处理均能提高小鼠肝脏中总超氧化物歧化酶(T-SOD)活性、过氧化氢酶(CAT)活性、谷胱甘肽(GSH)含量和总抗氧化能力(T-AOC),有效抑制丙二醛(MDA)的产生,减轻小鼠肝脏氧化损伤。其中,LC处理小鼠肝脏GSH含量、T-AOC分别比LUT处理增加5066%、3923%,MDA含量降低4104%。与CCl4处理相比,LUT、C3G、LC处理均能提高Nrf2、NQO1和HO-1基因的表达水平,降低Keap1基因的表达水平,其中,LC处理Nrf2、NQO1、HO-1基因相对表达量分别比LUT处理上调5740%、4650%、4277%,Keap1基因相对表达量下调4088%。LUT、C3G、LC处理能显著增加短链脂肪酸(SCFA)的产生,并增加肠道理研菌科(Rikenellaceae)和阿克曼氏菌科(Akkermansiaceae)细菌的相对丰度,而抗生素预处理则能干扰LUT和C3G对肠道菌群的调控,降低肠道毛螺菌科(Lachnospiraceae)和类杆菌科(Bacteroidaceae)细菌的相对丰度。综上,LUT和C3G联合使用能增强小鼠肝脏抗氧化酶活性、调控Nrf2信号通路基因表达水平以及改善肠道菌群结构。
Abstract:
To analyze the mechanism of action of lutein (LUT) and cyanidin-3-O-glucoside (C3G) alone and in combination on liver oxidative damage, this study constructed a mouse liver oxidative damage model induced by carbon 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 CCl4 treatment, LUT, C3G and LC treatments increased the activities of total superoxide dismutase (T-SOD) and catalase (CAT), elevated glutathione (GSH) content and total antioxidant capacity (T-AOC) in the liver of mice, and effectively inhibited the production of malondialdehyde (MDA), thereby alleviating hepatic oxidative damage in mice. Compared with the LUT-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 41.04%. Compared with CCl4 treatment, LUT, C3G and LC treatments could increase the expression levels of Nrf2, NQO1 and HO-1 genes and decrease the expression level of Keap1 gene. The relative expression levels of Nrf2, NQO1 and HO-1 genes in LC treatment were 57.40%, 46.50% and 42.77% higher than those in LUT treatment, while the relative expression level of Keap1 gene was down-regulated by 40.88%. LUT, C3G and LC treatments significantly increased the production of short-chain fatty acids (SCFA) and the relative abundance of Rikenellaceae and Akkermansia bacteria, while antibiotic pretreatment could interfere with the regulation of LUT and C3G on gut microbiota and reduce the relative abundance of Lachnospiraceae and Bacteroidaceae bacteria. In summary, the combined use of LUT and C3G can enhance the activty of antioxidant enzymes in the liver of mice, regulate the expression levels of Nrf2 pathway regulatory genes and improve the gut microbiota structure of mice.

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备注/Memo

备注/Memo:
收稿日期:2024-12-10基金项目:江苏省科技计划专项资金项目(BN2023060)作者简介:陆风芹(2000-),女,江苏盐城人,硕士研究生,主要从事食品营养研究。(E-mail)1537133799@qq.com通讯作者:张钟元,(E-mail)zzyszy2012@163.com
更新日期/Last Update: 2025-12-18