The effects of dietary pyridoxine (PN) on the gill immunity, apoptosis, antioxidant and tight junction of grass cap (Ctenopharyngodon idella) were investigated in this study. Fish were fed semi-purified diets containing graded levels of PN for 10 weeks, and then challenged with Flavobacterium columnare by bath immersion exposure for 3 days. The results indicated that compared with the optimal PN level, PN deficiency resulted in a decline in the antimicrobial compound production of gill. In addition, PN deficiency up-regulated the pro-inflammatory cytokines and down-regulated the anti-inflammatory cytokines gene expression, which might be associated with the enhanced nuclear factor κB p65 and the inhibited target of rapamycin signalling pathways, respectively, suggesting that PN deficiency could impair gill immune barrier function. Furthermore, PN deficiency (1) induced cell apoptosis, which may be partly associated with the (apoptotic protease activating factor-1, Bcl-2 associated X protein)/caspase-9 and c-Rel/tumor necrosis factor α (rather than FasL)/caspase-8 mediated apoptosis pathway. (2) Inhibited Kelch-like ECH-associating protein 1a/NF-E2-related factor 2 mRNA expression, decreased the mRNA expression and activities of antioxidant enzymes, increased the levels of reactive oxygen species, protein carbonyl and malondialdehyde. (3) Increased the mRNA expression level of myosin light chain kinase, which may be result in the down-regulation of tight junction complexes such as zonula occludens 1, occludin and claudins (expect claudin-12 and claudin-15). These results suggest that PN deficiency could impair gill physical barrier function. In summary, dietary PN deficiency could cause the impairment of gill barrier function associated with immunity, apoptosis, antioxidant and tight junction, which may result in the increased the susceptibility of fish to pathogenic bacteria. Moreover, based on the gill rot morbidity, LZ activity and MDA content, the dietary PN requirements for grass cap were estimated to be 4.85, 4.78 and 4.77 mg kg⁻¹ diet, respectively.

研究了膳食吡pyr醇（PN）对grass（Ctenopharyngodon idella）ill免疫，细胞凋亡，抗氧化剂和紧密连接的影响。给鱼喂半纯日粮，其中含PN分级，持续10周，然后用Flavobacterium columnare攻击。通过浸浴浸泡3天。结果表明，与最佳PN水平相比，PN缺乏导致g的抗菌化合物产量下降。另外，PN缺乏上调了促炎细胞因子的表达，下调了抗炎细胞因子的基因表达，这可能与核因子κBp65的增强和雷帕霉素信号通路的靶点抑制有关。缺乏会损害g免疫屏障功能。此外，PN缺乏（1）诱导细胞凋亡，这可能与（凋亡蛋白酶激活因子-1，Bcl-2相关X蛋白）/ caspase-9和c-Rel /肿瘤坏死因子α（而不是FasL）有关）/ caspase-8介导的凋亡途径。（2）抑制了Kelch样ECH相关蛋白1a / NF-E2相关因子2的mRNA表达，降低了mRNA的表达和抗氧化酶的活性，增加了活性氧，羰基蛋白和丙二醛的含量。（3）增加了肌球蛋白轻链激酶的mRNA表达水平，这可能导致紧密连接复合物（例如小带闭合，闭合蛋白和claudins）的下调（预期claudin-12和claudin-15）。这些结果表明，PN缺乏会损害g的物理屏障功能。总之，饮食中PN缺乏会导致与免疫，细胞凋亡，抗氧化剂和紧密连接相关的g屏障功能受损，这可能导致鱼类对病原菌的敏感性增加。而且，根据the腐病的发病率，^-1饮食。