학술논문
膳食核苷酸对SAMP8小鼠肝纤维化的改善作用 / Ameliorative Effect of Dietary Nucleotides on Liver Fibrosis in SAMP8 Mice
Document Type
Academic Journal
Author
Source
中国食物与营养 / Food and Nutrition in China. 29(9):67-72
Subject
Language
Chinese
ISSN
1006-9577
Abstract
目的:探讨膳食核苷酸对SAMP8小鼠肝脏纤维化的改善作用.方法:采用SPF级SAMP8小鼠48只,按体重随机分为正常对照组、核苷酸低剂量组、核苷酸中剂量组、核苷酸高剂量组,另取12只SAMR1小鼠作为模型对照组.正常对照组、模型对照组均采用基础饲料进行喂养,核苷酸低、中、高剂量组采用额外添加0.3、0.6、1.2 g/kg核苷酸的基础饲料进行喂养.所有组自3月龄开始干预,干预时长9个月.小鼠12月龄时,对小鼠肝组织进行HE染色观察肝脏组织病理学结构,检测肝脏羟脯氨酸、纤维化相关因子和氧化应激指标,同时选取正常对照组和核苷酸低剂量组进行转录组测序,对差异基因进行KEGG富集.结果:与模型对照组相比,正常对照组肝脏组织肝索结构紊乱,肝细胞排列不整齐,炎症细胞浸润.与正常对照组相比,膳食核苷酸显著改善了增龄性肝脏纤维化程度,提高肝脏SOD、GSH-Px活力,降低肝脏脂质过氧化物MDA水平.核苷酸还显著影响了细胞周期、氨基酸的生物合成和糖酵解/糖异生通路.结论:膳食核苷酸对SAMP8小鼠肝脏具有抗纤维化作用.
[Objective]To investigate the ameliorative effect of dietary nucleotides on liver fibrosis in SAMP8 mice.[Method]A total of 48 male specific pathogen free SAMP8 mice were randomly assigned into 4 groups,including control group,nucleotides low dose interven-tion group,nucleotides medium dose intervention group and nucleotides high dose intervention group.Totaly 12 3-month-old male SAMR1 nice were used as model control group.Control group and SAMR1 group were fed with basal diet,while low,medium and high nucleotides groups were fed with basal diet supplemented with 0.3 g/kg,0.6 g/kg and 1.2 g/kg nucleotides.All groups were treated from 3 months to 12 months of age.At the age of 12 months,the histopathological structure of liver was observed by HE staining,and the liver hydroxypro-line,fibrosis related factors and oxidative stress indexes were detected.Meanwhile,the control group and the low dose nucleotides group were selected for transcriptome sequencing,and the differential genes were enriched by KEGG.[Result]Compared with the model control group,the histological organization of the liver tissue in the control group exhibited increases of nuclear pyknosis,untidily organization of the hepatic cord,comprehensive hepatocellular ballooning,and several inflammatory cell infiltrations.Compared with control group,dieta-ry nucleotides significantly ameliorated the fibrosis of liver related aging,increased the activities of SOD and GSH-Px in liver,and de-creased the level of lipid peroxidase MDA in liver.Nucleotides also significantly affect cell cycle,biosynthesis of amino acids,and glycoly-sis/gluconeogenesis pathways.[Conclusion]Nucleotides can ameliorate liver fibrosis in SAMP8 mice
[Objective]To investigate the ameliorative effect of dietary nucleotides on liver fibrosis in SAMP8 mice.[Method]A total of 48 male specific pathogen free SAMP8 mice were randomly assigned into 4 groups,including control group,nucleotides low dose interven-tion group,nucleotides medium dose intervention group and nucleotides high dose intervention group.Totaly 12 3-month-old male SAMR1 nice were used as model control group.Control group and SAMR1 group were fed with basal diet,while low,medium and high nucleotides groups were fed with basal diet supplemented with 0.3 g/kg,0.6 g/kg and 1.2 g/kg nucleotides.All groups were treated from 3 months to 12 months of age.At the age of 12 months,the histopathological structure of liver was observed by HE staining,and the liver hydroxypro-line,fibrosis related factors and oxidative stress indexes were detected.Meanwhile,the control group and the low dose nucleotides group were selected for transcriptome sequencing,and the differential genes were enriched by KEGG.[Result]Compared with the model control group,the histological organization of the liver tissue in the control group exhibited increases of nuclear pyknosis,untidily organization of the hepatic cord,comprehensive hepatocellular ballooning,and several inflammatory cell infiltrations.Compared with control group,dieta-ry nucleotides significantly ameliorated the fibrosis of liver related aging,increased the activities of SOD and GSH-Px in liver,and de-creased the level of lipid peroxidase MDA in liver.Nucleotides also significantly affect cell cycle,biosynthesis of amino acids,and glycoly-sis/gluconeogenesis pathways.[Conclusion]Nucleotides can ameliorate liver fibrosis in SAMP8 mice