罗耳阿太菌多糖经Nrf2通路预防小鼠肝脏铅损伤机制  

Mechanism of Athelia rolfsii Polysaccharides Protect against Liver Injury in Lead-Exposed Mice via Nrf2 Signaling Pathway

作　　者：赵盼 李鸿梅[1] 王志超 闵伟红[1] ZHAO Pan;LI Hongmei;WANG Zhichao;MIN Weihong(College of Food Science and Engineering,Jilin Agricultural University,Changchun 130118,China)

机构地区：[1]吉林农业大学食品科学与工程学院,吉林长春130118

出　　处：《食品工业科技》2022年第20期395-402,共8页Science and Technology of Food Industry

摘　　要：目的:本研究旨在探究罗耳阿太菌多糖(Athelia rolfsii polysaccharides,AEPS)保护铅暴露小鼠肝脏的作用机制。方法:小鼠随机分为正常组(NC)、模型组(MC)、阳性对照组(PC)、AEPS低剂量组(LD)、AEPS中剂量组(MD)、AEPS高剂量组(HD)、全反式维甲酸(all-trans-retinoic acid,ATRA)单独组(ATRA+NC)、ATRA干预组(ATRA+MC)和ATRA+AEPS高剂量组(ATRA+HD)。测定铅暴露小鼠肝脏的铅含量、抗氧化指标、功能指标,苏木伊红染色评估小鼠肝脏病理切片。测定小鼠肝脏谷胱甘肽巯基转移酶(glutathione-s-transferase,GST)活性和谷胱甘肽(glutathione,GSH)水平,肝脏组织中细胞凋亡相关蛋白、多药耐药相关蛋白2(multidrug resistance-associated protein 2,MRP2)及肝细胞核中核因子E2相关因子2(nuclear factor erythroid-2-related factor 2,Nrf2)蛋白水平。结果:AEPS低、中、高剂量组均显著提高铅暴露小鼠肝细胞MRP2运输铅离子的能力(P<0.05),并呈剂量依赖性地减少小鼠肝脏铅积累(P<0.05)。AEPS显著抑制铅暴露小鼠肝细胞凋亡(P<0.05),呈剂量依赖性地增强小鼠肝脏抗氧化能力(P<0.05),恢复肝功能(P<0.05),并减轻肝脏病理损伤。AEPS还促进了Nrf2向肝细胞核转移(P<0.05)。而ATRA干预可降低AEPS对铅暴露小鼠肝脏的保护作用。结论:AEPS依赖于Nrf2信号通路可减少肝脏铅积累,保护肝脏铅损伤。Objective:The study aimed to explore the mechanism of Athelia rolfsii polysaccharides(AEPS)protected against liver of lead-exposed mice.Methods:Mice were randomly assigned into normal control group(NC),model control group(MC),positive control group(PC),AEPS low dose group(LD),AEPS middle dose group(MD),AEPS high dose group(HD),ATRA alone group(ATRA+NC),ATRA intervention group(ATRA+MC),ATRA+AEPS high dose group(ATRA+HD).Lead levels,antioxidant indexes and functional indexes in the liver of lead-exposed mice were determined,the pathological changes were also evaluated by hematoxylin-eosin(HE)staining.The activity of glutathione-s-transferase(GST)and the levels of glutathione(GSH)were also measured.The protein levels of apoptosis-associated proteins and multidrug resistance-associated protein 2(MRP2)in liver tissues were determined,as well as nuclear factor erythroid-2-related factor 2(Nrf2)in liver cell nucleus.Results:Low,middle and high dose of AEPS enhanced the lead ion excretion ability of MRP2 participation,decreased lead accumulation in mice liver significantly in a dose dependent manner(P<0.05).AEPS enhanced antioxidant activity of mice liver(P<0.05),restored liver function(P<0.05),alleviated liver pathological injury induced by lead in a dose dependent manner,as well as suppressed hepatocyte apoptosis of lead-exposed mice significantly(P<0.05).AEPS also promoted Nrf2 nuclear translocation in the liver(P<0.05).However,ATRA reduced the protective efficacy of AEPS on the liver of lead-exposed mice.Conclusion:AEPS reduced lead accumulation in the liver in a Nrf2-dependent manner,and showed liver protective effect.

关 键 词：罗耳阿太菌多糖(AEPS) 核因子E2相关因子2(Nrf2) 保护机制 铅暴露 肝脏损伤 

分 类 号：TS201.2[轻工技术与工程—食品科学]