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日粮 α-酮戊二酸缓解了大豆球蛋白和β-伴大豆球蛋白对鲫鱼()肠道的损伤。

Dietary α-ketoglutarate alleviates glycinin and β-conglycinin induced damage in the intestine of mirror carp ().

机构信息

College of Life Science, Huzhou University, Huzhou, China.

Nation Local Joint Engineering Laboratory of Aquatic Animal Genetic Breeding and Nutrition, Zhejiang Provincial Key Laboratory of Aquatic Bioresource Conservation and Development Technology, Huzhou, China.

出版信息

Front Immunol. 2023 Apr 28;14:1140012. doi: 10.3389/fimmu.2023.1140012. eCollection 2023.

DOI:10.3389/fimmu.2023.1140012
PMID:37187750
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10179059/
Abstract

This study investigated the glycinin and β-conglycinin induced intestinal damage and α-ketoglutarate alleviating the damage of glycinin and β-conglycinin in intestine. Carp were randomly divided into six dietary groups: containing fish meal (FM) as the protein source, soybean meal (SM), glycinin (FMG), β-conglycinin (FMc), glycinin+1.0% α-ketoglutarate (AKG) (FMGA), β-conglycinin+1.0% AKG (FMcA). The intestines were collected on 7, and the hepatopancreas and intestines were collected on 56. Fish treated with SM and FMc displayed reduced weight gain, specific growth rate, and protein efficiency. On 56 day, Fish fed on SM, FMG and FMc presented lower superoxide dismutase (SOD) activities. FMGA and FMcA had higher SOD activity than those fed on the FMG and FMc, respectively. In intestine, fish fed on the SM diets collected on 7 presented upregulated the expression of transforming growth factor beta (TGFβ1), AMP-activated protein kinase beta (AMPKβ), AMPKγ, and acetyl-CoA carboxylase (ACC). Fish fed FMG presented upregulated expression of tumor necrosis factor alpha (TNF-α), caspase9, and AMPKγ, while downregulated the expression of claudin7 and AMPKα. FMc group presented upregulated expression of TGFβ1, caspase3, caspase8, and ACC. Fish fed FMGA showed upregulated expression of TGFβ1, claudin3c, claudin7, while downregulating the expression of TNF-α and AMPKγ when compared to fish fed FMG diet. FMcA upregulated the expression of TGFβ1, claudin3c than fed on the FMc. In intestine, the villus height and mucosal thickness of the proximal intestine (PI) and the distal intestine (DI) were decreased and crypt depth of the PI and mid intestine (MI) were increased in SM, FMG and FMc. In addition, fish fed on SM, FMG and FMc presented lower citrate synthase (CS), isocitrate dehydrogenase (ICD), α-ketoglutarate dehydrogenase complex (α-KGDHC) Na/K-ATPase activity in DI. FMGA had higher CS, ICD, α-KGDHC, and Na/K-ATPase activity in PI and MI than those fed on the FMG. FMcA had higher Na/K-ATPase activity in MI. In conclusion, dietary soybean meal destroys the intestine's health, the adverse effects are related to the presence of β-conglycinin and glycinin, especially glycinin. AKG may regulate intestinal energy tricarboxylic acid cycle, thereby alleviating the damage intestinal morphology caused by the dietary soybean antigen proteins.

摘要

本研究旨在探讨大豆球蛋白和β-伴大豆球蛋白诱导的肠道损伤,以及α-酮戊二酸对肠内大豆球蛋白和β-伴大豆球蛋白损伤的缓解作用。鲤鱼被随机分为六组日粮:含鱼粉(FM)作为蛋白质源,豆粕(SM),大豆球蛋白(FMG),β-伴大豆球蛋白(FMc),大豆球蛋白+1.0%α-酮戊二酸(AKG)(FMGA),β-伴大豆球蛋白+1.0%AKG(FMcA)。第 7 天和第 56 天采集肠道,第 56 天采集肝胰腺和肠道。用 SM 和 FMc 喂养的鱼表现出体重增加、特定生长率和蛋白质效率降低。第 56 天,用 SM、FMG 和 FMc 喂养的鱼超氧化物歧化酶(SOD)活性较低。与单独用 FMG 或 FMc 喂养的鱼相比,用 FMGA 和 FMcA 喂养的鱼的 SOD 活性更高。在肠道中,第 7 天用 SM 日粮喂养的鱼上调了转化生长因子β(TGFβ1)、AMP 激活蛋白激酶β(AMPKβ)、AMPKγ 和乙酰辅酶 A 羧化酶(ACC)的表达。用 FMG 喂养的鱼上调了肿瘤坏死因子α(TNF-α)、caspase9 和 AMPKγ 的表达,而下调了 Claudin7 和 AMPKα 的表达。FMc 组上调了 TGFβ1、caspase3 和 caspase8 的表达,以及 ACC 的表达。与单独用 FMG 喂养的鱼相比,用 FMGA 喂养的鱼上调了 TGFβ1、claudin3c 的表达,而下调了 TNF-α和 AMPKγ 的表达。与单独用 FMc 喂养的鱼相比,用 FMcA 喂养的鱼上调了 TGFβ1、claudin3c 的表达。在肠道中,SM、FMG 和 FMc 降低了近端肠(PI)和远端肠(DI)的绒毛高度和黏膜厚度,增加了 PI 和中肠(MI)的隐窝深度。此外,用 SM、FMG 和 FMc 喂养的鱼在 DI 中的柠檬酸合成酶(CS)、异柠檬酸脱氢酶(ICD)、α-酮戊二酸脱氢酶复合体(α-KGDHC)和 Na/K-ATPase 活性较低。与单独用 FMG 喂养的鱼相比,用 FMGA 喂养的鱼在 PI 和 MI 中的 CS、ICD、α-KGDHC 和 Na/K-ATPase 活性更高。FMcA 喂养的鱼在 MI 中的 Na/K-ATPase 活性更高。综上所述,日粮豆粕破坏了肠道健康,其不良影响与β-伴大豆球蛋白和大豆球蛋白的存在有关,尤其是大豆球蛋白。AKG 可能通过调节肠道能量三羧酸循环,从而缓解日粮大豆抗原蛋白对肠道形态造成的损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/604e/10179059/2fdf6b1a3eb5/fimmu-14-1140012-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/604e/10179059/17a026ab45e9/fimmu-14-1140012-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/604e/10179059/5afd989b4aa2/fimmu-14-1140012-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/604e/10179059/2fdf6b1a3eb5/fimmu-14-1140012-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/604e/10179059/8f51ada612ce/fimmu-14-1140012-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/604e/10179059/f2af019afdf3/fimmu-14-1140012-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/604e/10179059/4c5bea5cef91/fimmu-14-1140012-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/604e/10179059/3e3d8027812b/fimmu-14-1140012-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/604e/10179059/17a026ab45e9/fimmu-14-1140012-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/604e/10179059/5afd989b4aa2/fimmu-14-1140012-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/604e/10179059/2fdf6b1a3eb5/fimmu-14-1140012-g008.jpg

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