Comparative proteomic analysis of liver antioxidant mechanisms in Megalobrama amblycephala stimulated with dietary emodin
文献类型： 外文期刊
作者： Song, Changyou 1 ; Liu, Bo 1 ; Xie, Jun 1 ; Ge, Xianping 1 ; Zhao, Zhenxin 1 ; Zhang, Yuanyuan 1 ; Zhang, Huimin 1 ; Ren, 1 ;
作者机构： 1.Nanjing Agr Univ, Wuxi Fisheries Coll, 9 Shanshui East Rd, Wuxi 214081, Peoples R China
2.Chinese Acad Fishery Sci, Minist Agr, Freshwater Fisheries Res Ctr, Key Lab Freshwater Fisheries & Germplasm Resource, Wuxi 214081, Peoples R China
期刊名称：SCIENTIFIC REPORTS （ 影响因子：4.379； 五年影响因子：5.133 ）
ISSN： 2045-2322
年卷期： 2017 年 7 卷
页码：
收录情况： SCI
摘要： Oxidative stress is a toxicological endpoint that correlates with the nutrition status of fish through cellular damage, inflammation, and apoptosis. In order to understand the antioxidant mechanism induced by dietary emodin in Megalobrama amblycephala liver, a comparative proteomic analysis was performed to investigate the proteome alteration under emodin administration. 27 altered protein spots were separated under 30 mg kg(-1) emodin stimulation based on 2-DE, and were all successfully identified using MALDI-TOF/TOF, representing 17 unique proteins. These proteins were functionally classified into antioxidant, metabolism, cytoskeleton, chaperone, signal transduction and cofactor groups. Network interaction and Gene Ontology annotation indicated 10 unique proteins were closely related to antioxidation and directly regulated by each other. Compared with the control group, administration of 30 mg kg(-1) emodin significantly increased the antioxidant-related mRNA expressions of GPx1, GSTm and HSP70, but decreased the mRNA expressions of GAPDH and Sord, which was consistent with the protein expression. Nevertheless, Pgk1 and Aldh8a1 were up-and down-regulated, and ALDOB was down-and up-regulated at the mRNA and protein levels, respectively. These results revealed that the altered proteins enhanced antioxidation via complex regulatory mechanisms, and 30 mg kg(-1) emodin was a suitable immunostimulant for M. amblycephala.
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