This study was conducted to explore the beneficial role of taurine against chronic high carbohydrate diet-induced oxidative stress, endoplasmic reticulum (ER) stress and inflammation, and to understand the underlying molecular mechanisms in turbot. Two 10-week feeding trials were simultaneously conducted. For the one, six experimental diets with graded levels of taurine supplementation (0, 0.4%, 0.8%, 1.2%, 1.6% and, 2.0%, respectively) and 15% of carbohydrate were used. For the other one, three graded levels of dietary taurine supplementation (0.4%, 1.2% and 2.0%, respectively) with 21% of carbohydrate were used. The results showed that higher expression level of inflammation cytokines and ER stress related genes were detected in higher dietary carbohydrate group. In both feeding trials, 1.2% of dietary taurine supplementation improved anti-oxidative status by decreasing the content of malondialdehyde, increasing the catalase activity and total anti-oxidative capacities. In feeding trial 1, appropriate taurine supplementation lowered contents of tumour necrosis factor-a, interleukin-6, aspartate aminotransferase and alkaline phosphatase in plasma, and decreased the expressions of pro-inflammatory cytokines, such as interleukin-8 (il-8) and interferon‐γ (ifn-γ). Furthermore, dietary taurine reduced ER stress by decreasing the mRNA levels of activating transcription factor 6, protein kinase R-like endoplasmic reticulum kinase and G protein-coupled receptor 78. The optimal dietary taurine content was estimated as 1.40% based on the analysis of specific growth rate. In feeding trial 2, dietary taurine supplementation attenuated liver inflammation partly referring to significantly down-regulated mRNA levels of nuclear transcription factor‐κB p65, ifn-γ, interleukin1β and up-regulate the transcript of ribosomal protein S6 kinase 1. Dietary taurine supplementation in feeding trial 2 significantly increased the Nrf2-related factor 2 protein level and decreased the NFκB p65 protein level only at 21% of dietary carbohydrate level. Taurine can alleviate the oxidative damage and inflammation caused by 21% of dietary carbohydrate to a certain degree. Overall, the present study confirmed that dietary taurine supplementation improved growth performance and anti-oxidative response, and reduced liver inflammatory and ER stress processes induced by high dietary carbohydrate in turbot.

进行这项研究以探讨牛磺酸对慢性高碳水化合物饮食引起的氧化应激，内质网（ER）应激和炎症的有益作用，并了解大菱t的潜在分子机制。同时进行了两个10周的喂养试验。对于其中的一种，使用了六种具有分级牛磺酸补充水平（分别为0、0.4％，0.8％，1.2％，1.6％和2.0％）和15％碳水化合物的实验饮食。对于另一种，使用三个等级的含21％碳水化合物的牛磺酸膳食补充剂（分别为0.4％，1.2％和2.0％）。结果表明，高碳水化合物饮食组中炎症细胞因子和内质网应激相关基因的表达水平较高。在两项喂养试验中，1。饮食中添加2％的牛磺酸可降低丙二醛含量，增加过氧化氢酶活性和总抗氧化能力，从而改善抗氧化状态。在喂养试验1中，适当补充牛磺酸可降低血浆中肿瘤坏死因子-a，白介素6，天冬氨酸转氨酶和碱性磷酸酶的含量，并降低促炎细胞因子如白介素8的表达（il-8）和干扰素-γ（ifn-γ）。此外，饮食性牛磺酸通过降低活化转录因子6，蛋白激酶R样内质网激酶和G蛋白偶联受体78的mRNA水平来降低内质网应激。根据特异性蛋白分析，最佳饮食性牛磺酸含量为1.40％增长率。在喂养试验2中，补充牛磺酸饮食可减轻肝脏炎症，部分原因是核转录因子κBp65，ifn-γ的mRNA水平显着下调，白细胞介素1β并上调核糖体蛋白S6激酶1的转录。饲喂试验2中补充牛磺酸可显着增加Nrf2相关因子2的蛋白水平，而降低NFκBp65的蛋白水平仅占饮食碳水化合物水平的21％。牛磺酸可以在一定程度上减轻由21％的饮食碳水化合物引起的氧化损伤和炎症。总的来说，本研究证实膳食牛磺酸补充剂可改善生长性能和抗氧化反应，并减少大菱t中高膳食碳水化合物诱导的肝脏炎症和内质网应激过程。