β-glucan regulates the intestinal immunity of pearl gentian grouper via the nuclear factor kappa B signaling pathway

IF 4.1 2区农林科学 Q1 FISHERIES

Fish & shellfish immunology Pub Date : 2024-10-04 DOI:10.1016/j.fsi.2024.109941

Fan Wang , Jia Xu , Chaoqun Hu , Junxiang Lai , Peihong Shen , Yishan Lu , Fajun Jiang

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引用次数: 0

Abstract

The preceding study observed that yeast β-glucan supplementation enhanced intestinal health and augmented disease resistance in pearl gentian grouper (Epinephelus lanceolatus♂ × Epinephelus fuscoguttatus♀), which occurred concurrently with the activation of the nuclear factor kappa B (NFκB) signaling pathway. Thus, we hypothesized that β-glucan improves intestinal health in grouper by modulating the NFκB pathway. Accordingly, the present study examined the effects of NFκB pathway disruption using a specific inhibitor on the intestinal health of pearl gentian grouper that had been injected with β-glucan. The experimental groups were as follows, (1) CD group: PBS injected; (2) βG group: β-glucan injected at a dose of 80 mg/kg; (3) PDTC group: NFκB inhibitor PDTC injected at a dose of 30 mg/kg; (4) βG + PDTC group: a combination of β-glucan (80 mg/kg) and PDTC (30 mg/kg) injected together. The results demonstrated that β-glucan-induced increases in mRNA expression levels of NFκB inhibitor α (iκbα) and p65, the degradation and phosphorylation of IκBα, and the phosphorylation of NFκB p65 were significantly inhibited following NFκB inhibition using PDTC in the intestine of grouper. The PDTC injection resulted in a significant reduction in the β-glucan-induced increase in mucin levels. The β-glucan-induced elevation of alkaline phosphatase (AKP) activity, component 3 (C3) content, and inflammatory factors were significantly suppressed following NFκB inhibition. The βG + PDTC treatment resulted in a restoration of catalase (CAT) enzyme activity to the level observed in the CD treatment, while total antioxidant capacity (T-AOC) was decreased to the level of the βG treatment. The β-glucan-induced downregulation of caspase8 (casp8) was reversed following NFκB inhibition, as well as the mRNA levels of casp3 and casp9 being elevated to a greater extent. In conclusion, the β-glucan-regulated intestinal immunity in grouper may be mediated by the NFκB pathway. Furthermore, the inhibitory effect of β-glucan on apoptosis and oxidative stress may not be related to the NFκB signaling pathway.

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β-葡聚糖通过核因子卡巴B信号通路调节珍珠龙胆石斑鱼的肠道免疫力

前一项研究观察到，补充酵母β-葡聚糖可增强珍珠龙胆石斑鱼（Epinephelus lanceolatus♂ × Epinephelus fuscoguttatus♀）的肠道健康和抗病能力，而这与核因子卡巴B（NFκB）信号通路的激活同时发生。因此，我们假设β-葡聚糖通过调节NFκB通路来改善石斑鱼的肠道健康。因此，本研究使用一种特异性抑制剂来检测NFκB通路中断对注射了β-葡聚糖的珍珠龙胆石斑鱼肠道健康的影响。实验组如下：（1）CD 组：注射 PBS；(2) βG 组：注射 β-葡聚糖，剂量为 80 mg/kg；(3) PDTC 组：(3) PDTC 组：注射 NFκB 抑制剂 PDTC，剂量为 30 mg/kg；(4) βG+ PDTC 组：同时注射 β-葡聚糖（80 mg/kg）和 PDTC（30 mg/kg）。结果表明，使用 PDTC 抑制 NFκB 后，β-葡聚糖诱导的石斑鱼肠道中 NFκB 抑制剂 α（iκbα）和 p65 mRNA 表达水平的增加、IκBα 的降解和磷酸化以及 NFκB p65 的磷酸化均受到显著抑制。注射 PDTC 后，β-葡聚糖诱导的粘蛋白水平增加明显减少。抑制 NFκB 后，β-葡聚糖诱导的碱性磷酸酶（AKP）活性、3 号成分（C3）含量和炎症因子的升高明显受到抑制。βG+PDTC处理使过氧化氢酶（CAT）活性恢复到CD处理时的水平，而总抗氧化能力（T-AOC）则下降到βG处理时的水平。抑制 NFκB 后，β-葡聚糖诱导的 caspase8（casp8）下调被逆转，casp3 和 casp9 的 mRNA 水平也有较大程度的升高。总之，β-葡聚糖调控的石斑鱼肠道免疫可能是由 NFκB 通路介导的。此外，β-葡聚糖对细胞凋亡和氧化应激的抑制作用可能与 NFκB 信号通路无关。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Fish & shellfish immunology 农林科学-海洋与淡水生物学

CiteScore

7.50

自引率

19.10%

发文量

750

审稿时长

68 days

期刊介绍： Fish and Shellfish Immunology rapidly publishes high-quality, peer-refereed contributions in the expanding fields of fish and shellfish immunology. It presents studies on the basic mechanisms of both the specific and non-specific defense systems, the cells, tissues, and humoral factors involved, their dependence on environmental and intrinsic factors, response to pathogens, response to vaccination, and applied studies on the development of specific vaccines for use in the aquaculture industry.