我们之前的研究表明，补充酵母β-葡聚糖可以改善珍珠龙胆石斑鱼（Epinephelus lanceolatus♂ × Epinephelus fuscoguttatus♀）的肠道健康，同时激活丝裂原激活蛋白激酶（MAPK）信号通路。在这项研究中，我们研究了使用抑制剂干扰 p38 MAPK 活性对注射 β-葡聚糖的珍珠龙胆石斑鱼肠道健康的影响，以阐明 β-葡聚糖对鱼肠道保护作用的潜在分子机制。将珍珠龙胆石斑鱼分为四组：注射PBS（CD组）、注射80mg/kg的β-葡聚糖（βG组）、注射1mg/kg的p38 MAPK抑制剂SB203580（SB203580组） ），以及一起注射β-葡聚糖（80 mg/kg）和SB203580（1 mg/kg）的组合（βG SB203580组）。结果表明，SB203580 的引入显着抑制了 β-葡聚糖诱导的 p38α 和 p38β mRNA 表达的增加，以及 p38 MAPK 的磷酸化。 βG组和SB203580组均表现出皱襞高度和肌层厚度的降低。 βG SB203580组显示粘蛋白细胞水平显着降低；白细胞介素 1β (il1β) mRNA 表达；诱导一氧化氮合酶、肿瘤坏死因子α和IL1β浓度；过氧化氢酶和总抗氧化能力活性。此外，与βG组相比，βG SB203580组的肠道丙二醛水平显着增加。 p38 MAPK 信号传导的抑制阻止了 β-葡聚糖诱导的凋亡相关 caspase 分子表达的趋势。总之，注射β-葡聚糖通过调节p38 MAPK通路导致石斑鱼粘液细胞、非特异性免疫、抗氧化能力和抗凋亡水平升高。这项研究深入探讨了 β-葡聚糖对珍珠龙胆石斑鱼肠道健康的保护作用的潜在分子机制。版权所有 © 2024。由 Elsevier Ltd 出版。

Our previous study has demonstrated that supplementation of yeast β-glucan improves intestinal health in pearl gentian grouper (Epinephelus lanceolatus♂ × Epinephelus fuscoguttatus♀), accompanied by the activation of the mitogen-activated protein kinase (MAPK) signaling pathway. In this study, we investigated the effects of perturbing p38 MAPK activity using an inhibitor on the intestinal health of β-glucan-injected pearl gentian grouper to elucidate the potential molecular mechanism underlying the protective effects of β-glucan on the fish gut. The pearl gentian grouper was categorized into four groups: PBS injected (CD group), β-glucan injected at a dose of 80 mg/kg (βG group), p38 MAPK inhibitor SB203580 injected at a dose of 1 mg/kg (SB203580 group), and a combination of β-glucan (80 mg/kg) and SB203580 (1 mg/kg) injected together (βG+SB203580 group). The results revealed that the introduction of SB203580 significantly suppressed the β-glucan-induced increase in p38α and p38β mRNA expression, as well as the phosphorylation of p38 MAPK. Both the βG group and SB203580 group exhibited reduced plica height and muscularis thickness. The βG+SB203580 group displayed a significant reduction in mucin cell level; interleukin 1β (il1β) mRNA expression; induced nitric oxide synthase, tumor necrosis factor α, and IL1β concentration; catalase and total antioxidant capacity activities. Additionally, there was a significant increase in the levels of intestinal malondialdehyde in the βG+SB203580 group compared to the βG group. The inhibition of the p38 MAPK signaling halted the trend of apoptosis-related caspase molecular expression induced by β-glucan. In conclusion, β-glucan injection resulted in elevated levels of mucous cells, nonspecific immunity, antioxidant capacity, and anti-apoptosis in grouper by modulating the p38 MAPK pathway. This study offers insights into the potential molecular mechanism underlying the protective effects of β-glucan on intestinal health in pearl gentian grouper.Copyright © 2024. Published by Elsevier Ltd.