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膳食姜黄素减轻赭曲霉毒素A诱导的草鱼幼鱼肠道损伤:坏死性凋亡和炎症反应

Dietary curcumin alleviates intestinal damage induced by ochratoxin A in juvenile grass carp (): Necroptosis and inflammatory responses.

作者信息

Zhao Piao, Jiang Wei-Dan, Wu Pei, Liu Yang, Ren Hong-Mei, Jin Xiao-Wan, Feng Lin, Zhou Xiao-Qiu

机构信息

Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, Sichuan, China.

Fish Nutrition and Safety Production University Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu 611130, Sichuan, China.

出版信息

Anim Nutr. 2024 May 1;18:119-132. doi: 10.1016/j.aninu.2024.04.011. eCollection 2024 Sep.

DOI:10.1016/j.aninu.2024.04.011
PMID:39263441
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11388201/
Abstract

Ochratoxin A (OTA) is one of the most common pollutants in aquatic feed. As a first line of defense, intestinal barriers could be utilized against OTA in order to prevent disorders. Natural product supplementation is one of the most popular strategies to alleviate toxicity induced by mycotoxins, but there is a lack of knowledge about how it functions in the teleost intestine. In this study, 720 juvenile grass carp of about 11 g were selected and four treatment groups (control group, OTA group, curcumin [Cur] group, and OTA + Cur group) were set up to conduct a 60-day growth test. After the test, the growth performance and intestinal health related indexes of grass carp were investigated. The addition of dietary Cur could have the following main results: (1) inhibit absorption and promote efflux transporters mRNA expression, reducing the residuals of OTA, (2) decrease oxidative stress by reducing oxidative damage and enhancing the expression of antioxidant enzymes, (3) promote mitochondrial fusion proteins to inhibit the expression of mitotic proteins and mitochondrial autophagy proteins and enhance mitochondrial function, (4) reduce necroptosis-related gene expression through inhibiting the tumor necrotic factor receptor-interacting protein kinase/mixed lineage kinase domain-like pathway, (5) reduce the expression of pro-inflammatory factors by inhibiting the Toll-like receptor 4/nuclear factor-κB signaling pathway to alleviate the intestinal inflammatory response. In summary, the results suggested that Cur could alleviate OTA-induced intestinal damage by enhancing antioxidant capacity and mitochondrial function as well as reducing necroptosis and inflammation in the grass carp intestine. This study provided a theoretical basis and production implications for dietary Cur that could improve growth performance and alleviate the intestinal damage induced by OTA in fish.

摘要

赭曲霉毒素A(OTA)是水产饲料中最常见的污染物之一。作为第一道防线,肠道屏障可用于抵御OTA以预防疾病。补充天然产物是减轻霉菌毒素诱导毒性的最常用策略之一,但对于其在硬骨鱼肠道中的作用机制尚缺乏了解。本研究选取720尾体重约11 g的草鱼幼鱼,设置四个处理组(对照组、OTA组、姜黄素[Cur]组和OTA + Cur组)进行为期60天的生长试验。试验结束后,对草鱼的生长性能和肠道健康相关指标进行了研究。饲料中添加Cur可能产生以下主要结果:(1)抑制吸收并促进外流转运蛋白mRNA表达,减少OTA残留;(2)通过减少氧化损伤和增强抗氧化酶表达来降低氧化应激;(3)促进线粒体融合蛋白表达以抑制分裂蛋白和线粒体自噬蛋白表达并增强线粒体功能;(4)通过抑制肿瘤坏死因子受体相互作用蛋白激酶/混合谱系激酶结构域样途径减少坏死性凋亡相关基因表达;(5)通过抑制Toll样受体4/核因子-κB信号通路减少促炎因子表达以减轻肠道炎症反应。综上所述,结果表明Cur可通过增强抗氧化能力和线粒体功能以及减少草鱼肠道中的坏死性凋亡和炎症来减轻OTA诱导的肠道损伤。本研究为日粮中添加Cur可改善鱼类生长性能并减轻OTA诱导的肠道损伤提供了理论依据和生产指导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/c662a2aa75a0/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/f3506f981492/gr1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/44b168704b9d/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/5c98b370fa9b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/f08f236df6f6/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/14ee01e356d4/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/139dddc4453e/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/0fa03f872853/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/c662a2aa75a0/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/f3506f981492/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/cfe798c3ea29/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/44b168704b9d/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/5c98b370fa9b/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/f08f236df6f6/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/14ee01e356d4/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/139dddc4453e/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/0fa03f872853/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acdb/11388201/c662a2aa75a0/gr9.jpg

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