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通过调节PI3K/AKT和脂肪酸代谢信号通路促进感染罗非鱼的存活。 (注:原文“by Regulating the PI3K/AKT and Fatty Acid Metabolism Signaling Pathway”前缺少具体病原体,翻译可能不完全准确,需结合完整原文信息理解。)

Promotes Survival of Tilapia Infected With by Regulating the PI3K/AKT and Fatty Acid Metabolism Signaling Pathway.

作者信息

Li Hong Xia, Qiang Jun, Song Chang You, Xu Pao

机构信息

Wuxi Fisheries College, Nanjing Agricultural University, Wuxi, China.

Key Laboratory of Freshwater Fisheries and Germplasm Resources Utilization, Ministry of Agriculture and Rural Affairs, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi, China.

出版信息

Front Physiol. 2021 Jul 9;12:699247. doi: 10.3389/fphys.2021.699247. eCollection 2021.

DOI:10.3389/fphys.2021.699247
PMID:34305652
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8299465/
Abstract

has greatly restricted the development of healthy tilapia aquaculture. As a green and efficient feed addition, (APS) has been increasingly used in culture, but it is unclear whether it represents a disease-resistant feed. Genetically improved farmed tilapia (GIFT, ) was fed with a feed supplemented with 0 (control), 0.5, 1, 2, 4, and 8‰ APS for 56 days, after which fish were injected with 5.9 × 10 CFU/ml into the abdominal cavity. At 96 h after infection, the cumulative survival of GIFT in control and 0.5‰ APS treatments was significantly lower than in other treatments; at APS supplementation rates of 1 and 2‰, serum glucose, triglycerides, and cholesterol contents were all significantly lower than in control treatment fish. Hepatic glycogen and triglyceride contents of 1‰ APS treatment fish were significantly higher than those in fish in control treatment. Transcription levels of peroxisome proliferator activated receptor α (PPAR), fatty acid synthase (FAS), and lipoprotein Lipase (LPL) genes were upregulated, and their expression levels in fish in 1, 2, and 4‰ treatments were significantly higher than those in fish in control treatment at 96 h after infection. After 96 h of infection, the red blood cells, hemoglobin, hematocrit, and white blood cells of fish in 1‰ APS treatment were significantly lower than those of fish in 4 and 8‰ treatments; hepatic catalase activity was activated at 48 h, superoxide dismutase activity was also significantly upregulated at 96 h, and the malondialdehyde content significantly decreased. It is noted that 0.5-2‰ APS treatments significantly activated the expression of PI3K and AKT in the liver, while inhibiting the expression of Caspase-9. Therefore, feed with 1‰ APS can promote hepatic glycogen and lipid metabolism in GIFT after infection with , which is beneficial to alleviating oxidative stress damage and cell apoptosis in liver tissue.

摘要

这极大地限制了罗非鱼健康养殖的发展。作为一种绿色高效的饲料添加剂,(APS)已在养殖中越来越多地被使用,但它是否是一种抗病饲料尚不清楚。对遗传改良养殖罗非鱼(GIFT)投喂添加0(对照)、0.5、1、2、4和8‰ APS的饲料56天,之后将5.9×10 CFU/ml 腹腔注射到鱼体内。感染后96小时,对照和0.5‰ APS处理组中GIFT的累积存活率显著低于其他处理组;在APS添加率为1和2‰时,血清葡萄糖、甘油三酯和胆固醇含量均显著低于对照处理的鱼。1‰ APS处理组鱼的肝糖原和甘油三酯含量显著高于对照处理组的鱼。过氧化物酶体增殖物激活受体α(PPAR)、脂肪酸合酶(FAS)和脂蛋白脂肪酶(LPL)基因的转录水平上调,在感染后96小时,1、2和4‰处理组鱼中它们的表达水平显著高于对照处理组的鱼。感染96小时后,1‰ APS处理组鱼的红细胞、血红蛋白、血细胞比容和白细胞显著低于4和8‰处理组的鱼;肝过氧化氢酶活性在48小时被激活,超氧化物歧化酶活性在96小时也显著上调,丙二醛含量显著降低。值得注意的是,0.5 - 2‰ APS处理显著激活了肝脏中PI3K和AKT的表达,同时抑制了Caspase - 9的表达。因此,添加1‰ APS的饲料在罗非鱼感染 后可促进其肝脏糖原和脂质代谢,这有利于减轻肝脏组织的氧化应激损伤和细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c23e/8299465/971a7fbb7022/fphys-12-699247-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c23e/8299465/85ba996db92e/fphys-12-699247-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c23e/8299465/c3374cf85e28/fphys-12-699247-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c23e/8299465/fcffa0a13b22/fphys-12-699247-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c23e/8299465/94718acff185/fphys-12-699247-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c23e/8299465/971a7fbb7022/fphys-12-699247-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c23e/8299465/85ba996db92e/fphys-12-699247-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c23e/8299465/c3374cf85e28/fphys-12-699247-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c23e/8299465/fcffa0a13b22/fphys-12-699247-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c23e/8299465/94718acff185/fphys-12-699247-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c23e/8299465/971a7fbb7022/fphys-12-699247-g005.jpg

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