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

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.