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氨氮胁迫会损害黄颡鱼的肠道黏膜屏障并引发肠道炎症。

Ammonia nitrogen stress damages the intestinal mucosal barrier of yellow catfish () and induces intestinal inflammation.

作者信息

Liu Senyue, Luo Lin, Zuo Fengyuan, Huang Xiaoli, Zhong Liang, Liu Sha, Geng Yi, Ou Yangping, Chen Defang, Cai Wenlong, Deng Yongqiang

机构信息

Fisheries Research Institute, Sichuan Academy of Agricultural Sciences, Chengdu, Sichuan, China.

2 Department of Aquaculture, College of Animal Science & Technology, Sichuan Agricultural University, Chengdu, Sichuan, China.

出版信息

Front Physiol. 2023 Sep 19;14:1279051. doi: 10.3389/fphys.2023.1279051. eCollection 2023.

Abstract

Nitrogen from ammonia is one of the most common pollutants toxics to aquatic species in aquatic environment. The intestinal mucosa is one of the key mucosal defenses of aquatic species, and the accumulation of ammonia nitrogen in water environment will cause irreversible damage to intestinal function. In this study, histology, immunohistochemistry, ultrastructural pathology, enzyme activity analysis and qRT-PCR were performed to reveal the toxic effect of ammonia nitrogen stress on the intestine of . According to histological findings, ammonia nitrogen stress caused structural damage to the intestine and reduced the number of mucous cells. Enzyme activity analysis revealed that the activity of bactericidal substances (Lysozyme, alkaline phosphatase, and ACP) had decreased. The ultrastructure revealed sparse and shortened microvilli as well as badly degraded tight junctions. Immunohistochemistry for ZO-1 demonstrated an impaired intestinal mucosal barrier. Furthermore, qRT-PCR revealed that tight junction related genes () were downregulated, while the pore-forming protein was upregulated. Furthermore, as ammonia nitrogen concentration grew, so did the positive signal of Zap-70 (T/NK cell) and the expression of inflammation-related genes (, , . In light of the above findings, we conclude that ammonia nitrogen stress damages intestinal mucosal barrier of and induces intestinal inflammation.

摘要

氨中的氮是水生环境中对水生物种最常见的有毒污染物之一。肠道黏膜是水生物种关键的黏膜防御屏障之一,水环境中氨氮的积累会对肠道功能造成不可逆转的损害。在本研究中,通过组织学、免疫组织化学、超微结构病理学、酶活性分析和qRT-PCR来揭示氨氮胁迫对[具体物种]肠道的毒性作用。根据组织学结果,氨氮胁迫导致肠道结构损伤,黏液细胞数量减少。酶活性分析表明,杀菌物质(溶菌酶、碱性磷酸酶和酸性磷酸酶)的活性降低。超微结构显示微绒毛稀疏且缩短,紧密连接严重降解。ZO-1的免疫组织化学显示肠道黏膜屏障受损。此外,qRT-PCR显示紧密连接相关基因([具体基因])下调,而成孔蛋白上调。此外,随着氨氮浓度的增加,Zap-70(T/NK细胞)的阳性信号以及炎症相关基因([具体基因])的表达也增加。鉴于上述发现,我们得出结论,氨氮胁迫会损害[具体物种]的肠道黏膜屏障并诱发肠道炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/482e/10542119/f12a0495dc95/fphys-14-1279051-g001.jpg

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