Liang Hualiang, Xu Pao, Xu Gangchun, Zhang Lin, Huang Dongyu, Ren Mingchun, Zhang Lu
Key Laboratory of Integrated Rice-Fish Farming Ecology, Ministry of Agriculture and Rural Affairs, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi 214081, China.
Wuxi Fisheries College, Nanjing Agricultural University, Wuxi 214081, China.
Antioxidants (Basel). 2022 Dec 2;11(12):2399. doi: 10.3390/antiox11122399.
This 56-day study aimed to evaluate the effects of histidine levels on intestinal antioxidant capacity and endoplasmic-reticulum stress (ERS) in largemouth bass (). The initial weights of the largemouth bass were (12.33 ± 0.01) g. They were fed six graded levels of histidine: 0.71% (deficient group), 0.89%, 1.08%, 1.26%, 1.48%, and 1.67%. The results showed that histidine deficiency significantly suppressed the intestinal antioxidant enzyme activities, including SOD, CAT, GPx, and intestinal level of GSH, which was supported by significantly higher levels of intestinal MDA. Moreover, histidine deficiency significantly lowered the mRNA level of and upregulated the mRNA level of , which further lowered the mRNA levels of the downstream genes , and . Additionally, histidine-deficiency-induced intestinal ERS, which was characterized by activating the PEPK-signalling pathway and IRE1-signalling pathway, including increased core gene expression of , , eif2α, , , , , , and . Dietary histidine deficiency also induced apoptosis and necroptosis in the intestine by upregulating the expressions of proapoptotic genes, including , , , and and necroptosis-related genes, including and , while also lowering the mRNA level of the antiapoptotic gene . Furthermore, histidine deficiency activated the NF-κB-signalling pathway to induce an inflammatory response, improving the mRNA levels of the proinflammatory factors , , , , and and lowering the mRNA levels of the anti-inflammatory factors and . Similarly, dietary histidine deficiency significantly lowered the intestinal levels of the anti-inflammatory factors TGF-β and IL-10 and upregulated the intestinal levels of the proinflammatory factor TNF-α, showing a trend similar to the gene expression of inflammatory factors. However, dietary histidine deficiency inhibited only the level of C3, and no significant effects were observed for IgM, IgG, HSP70, or IFN-γ. Based on the MDA and T-SOD results, the appropriate dietary histidine requirements of juvenile largemouth bass were 1.32% of the diet (2.81% dietary protein) and 1.47% of the diet (3.13% dietary protein), respectively, as determined by quadratic regression analysis.
这项为期56天的研究旨在评估组氨酸水平对大口黑鲈肠道抗氧化能力和内质网应激（ERS）的影响。大口黑鲈的初始体重为（12.33±0.01）克。它们被投喂六种不同梯度水平的组氨酸：0.71%（缺乏组）、0.89%、1.08%、1.26%、1.48%和1.67%。结果表明，组氨酸缺乏显著抑制了肠道抗氧化酶活性，包括超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPx）以及肠道谷胱甘肽（GSH）水平，这一点得到了肠道丙二醛（MDA）水平显著升高的支持。此外，组氨酸缺乏显著降低了[具体基因1]的mRNA水平，并上调了[具体基因2]的mRNA水平，这进一步降低了下游基因[具体基因3]、[具体基因4]和[具体基因5]的mRNA水平。此外，组氨酸缺乏诱导肠道ERS，其特征是激活磷酸烯醇丙酮酸羧激酶（PEPK）信号通路和肌醇需求酶1（IRE1）信号通路，包括[具体核心基因1]、[具体核心基因2]、真核翻译起始因子2α（eif2α）、[具体基因6]、[具体基因7]、[具体基因8]、[具体基因9]、[具体基因10]和[具体基因11]的核心基因表达增加。日粮组氨酸缺乏还通过上调促凋亡基因[具体促凋亡基因1]、[具体促凋亡基因2]、[具体促凋亡基因3]和[具体促凋亡基因4]以及坏死性凋亡相关基因[具体坏死性凋亡相关基因1]和[具体坏死性凋亡相关基因2]的表达诱导肠道凋亡和坏死性凋亡，同时也降低了抗凋亡基因[具体抗凋亡基因]的mRNA水平。此外，组氨酸缺乏激活核因子κB（NF-κB）信号通路以诱导炎症反应，提高促炎因子[具体促炎因子1]、[具体促炎因子2]、[具体促炎因子3]、[具体促炎因子4]和[具体促炎因子5]的mRNA水平，并降低抗炎因子[具体抗炎因子1]和[具体抗炎因子2]的mRNA水平。同样，日粮组氨酸缺乏显著降低了抗炎因子转化生长因子-β（TGF-β）和白细胞介素-10（IL-10）的肠道水平，并上调了促炎因子肿瘤坏死因子-α（TNF-α）的肠道水平，呈现出与炎症因子基因表达相似的趋势。然而，日粮组氨酸缺乏仅抑制了补体3（C3）的水平，而对免疫球蛋白M（IgM））、免疫球蛋白G（IgG）、热休克蛋白HSP70或干扰素-γ（IFN-γ）未观察到显著影响。基于丙二醛（MDA）和总超氧化物歧化酶（T-SOD）结果，通过二次回归分析确定，大口黑鲈幼鱼日粮中适宜的组氨酸需求量分别为日粮的1.32%（日粮蛋白质含量为2.81%）和1.47%（日粮蛋白质含量为3.13%）。
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