Guangxi Key Laboratory of Marine Environmental Science, Guangxi Academy of Marine Sciences, Guangxi Academy of Sciences, Nanning, China; College of Life Science and Technology of Guangxi University, Nanning, 530005, Guangxi, China.
Guangxi Key Laboratory of Marine Environmental Science, Guangxi Academy of Marine Sciences, Guangxi Academy of Sciences, Nanning, China.
Fish Shellfish Immunol. 2024 Nov;154:109941. doi: 10.1016/j.fsi.2024.109941. Epub 2024 Oct 4.
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.
上述研究观察到，酵母β-葡聚糖的补充增强了珍珠龙胆石斑鱼（Epinephelus lanceolatus♂×Epinephelus fuscoguttatus♀）的肠道健康并提高了其抗病能力，同时激活了核因子 kappa B（NFκB）信号通路。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，本研究使用特定的抑制剂来研究 NFκB 通路破坏对已注射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 80mg/kg 的β-葡聚糖；（3）PDTC 组：注射 30mg/kg 的 NFκB 抑制剂 PDTC；（4）βG+PDTC 组：同时注射 80mg/kg 的β-葡聚糖和 30mg/kg 的 PDTC。结果表明，在石斑鱼肠道中使用 PDTC 抑制 NFκB 后，β-葡聚糖诱导的 NFκB 抑制剂 α（IκBα）和 p65 的 mRNA 表达水平增加、IκBα 的降解和磷酸化以及 NFκB p65 的磷酸化均受到显著抑制。PDTC 注射导致β-葡聚糖诱导的粘蛋白水平升高显著降低。NFκB 抑制后，β-葡聚糖诱导的碱性磷酸酶（AKP）活性、补体 3（C3）含量和炎症因子的升高显著受到抑制。βG+PDTC 处理导致 CAT 酶活性恢复到 CD 处理水平，而总抗氧化能力（T-AOC）降低到βG 处理水平。NFκB 抑制后，β-葡聚糖诱导的 caspase8（casp8）下调得到逆转，同时 casp3 和 casp9 的 mRNA 水平升高到更高的程度。综上所述，β-葡聚糖调节石斑鱼肠道免疫可能是通过 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。
