High-Fat-Diet-Induced Oxidative Stress in Giant Freshwater Prawn (Macrobrachium rosenbergii) via NF-kappa B/NO Signal Pathway and the Amelioration of Vitamin E
文献类型： 外文期刊
作者： Sun, Cunxin 1 ; Shan, Fan 2 ; Liu, Mingyang 2 ; Liu, Bo 1 ; Zhou, Qunlan 1 ; Zheng, Xiaochuan 1 ; Xu, Xiaodi 2 ;
作者机构： 1.Chinese Acad Fishery Sci, Freshwater Fisheries Res Ctr, Key Lab Freshwater Fisheries & Germplasm Resource, Minist Agr & Rural Affairs, Wuxi 214081, Jiangsu, Peoples R China
2.Nanjing Agr Univ, Wuxi Fisheries Coll, Wuxi 214081, Jiangsu, Peoples R China
关键词： high fat diet; oxidative stress; NF-kappa B; vitamin E; Macrobrachium rosenbergii
期刊名称：ANTIOXIDANTS （ 影响因子：7.675； 五年影响因子：7.886 ）
ISSN：
年卷期： 2022 年 11 卷 2 期
页码：
收录情况： SCI
摘要： Lipids work as essential energy sources for organisms. However, prawns fed on high-fat diets suffer from oxidative stress, whose potential mechanisms are poorly understood. The present study aimed to explore the regulation mechanism of oxidative stress induced by high fat and the amelioration by vitamin E (VE) of oxidative stress. Macrobrachium rosenbergii were fed with two dietary fat levels (LF 9% and HF 13%) and two VE levels (200 mg/kg and 600 mg/kg) for 8 weeks. The results showed that the HF diet decreased the growth performance, survival rate and antioxidant capacity of M. rosenbergii, as well as inducing hypertrophied lipid droplets, lipophagy and apoptosis. A total of 600 mg/kg of VE in the HF diet alleviated the negative effects induced by HF. In addition, the HF diet suppressed the expression of toll-dorsal and imd-relish signal pathways. After the relish and dorsal pathways were knocked down, the downstream iNOS and NO levels decreased and the MDA level increased. The results indicated that M. rosenbergii fed with a high-fat diet could cause oxidative damage. Its molecular mechanism may be attributed to the fact that high fat suppresses the NF-kappa B/NO signaling pathway mediating pro-oxidant and antioxidant targets for regulation of oxidative stress. Dietary VE in an HF diet alleviated hepatopancreas oxidative stress and apoptosis.
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