硒 (Se) 是鱼类必需的微量元素之一,可调节免疫系统功能并维持免疫稳态。肌肉是产生运动和维持姿势的重要组织。目前关于缺硒对鲤鱼肌肉影响的研究较少。在本试验中,通过饲喂不同硒含量的日粮,成功建立了缺硒模型。低硒饮食导致肌肉硒含量降低。组织学分析表明,缺硒会导致肌纤维断裂、溶解、紊乱,并增加肌细胞凋亡。转录组显示总共筛选了 367 个差异表达基因 (DEG),包括 213 个上调的 DEG 和 154 个下调的 DEG。生物信息学分析表明,DEGs 集中在氧化还原过程中,炎症和细胞凋亡,并与 NF-κB 和 MAPKs 通路相关。进一步探索机制表明,硒缺乏导致ROS过度积累,抗氧化酶活性降低,同时也导致NF-κB和MAPKs通路表达增加。此外,硒缺乏显着增加TNF-α、IL-1β和IL-6以及促凋亡因子BAX、p53、caspase-7和caspase-3的表达,同时降低抗凋亡因子Bcl的表达-2 和 Bcl-xl。综上所述,缺硒降低了抗氧化酶的活性,导致ROS过度积累,引起氧化应激,影响鲤鱼的免疫功能,导致肌肉炎症和细胞凋亡。进一步探索机制表明,硒缺乏导致ROS过度积累,抗氧化酶活性降低,同时也导致NF-κB和MAPKs通路表达增加。此外,硒缺乏显着增加TNF-α、IL-1β和IL-6以及促凋亡因子BAX、p53、caspase-7和caspase-3的表达,同时降低抗凋亡因子Bcl的表达-2 和 Bcl-xl。综上所述,缺硒降低了抗氧化酶的活性,导致ROS过度积累,引起氧化应激,影响鲤鱼的免疫功能,导致肌肉炎症和细胞凋亡。进一步探索机制表明,硒缺乏导致ROS过度积累,抗氧化酶活性降低,同时也导致NF-κB和MAPKs通路表达增加。此外,硒缺乏显着增加TNF-α、IL-1β和IL-6以及促凋亡因子BAX、p53、caspase-7和caspase-3的表达,同时降低抗凋亡因子Bcl的表达-2 和 Bcl-xl。综上所述,缺硒降低了抗氧化酶的活性,导致ROS过度积累,引起氧化应激,影响鲤鱼的免疫功能,导致肌肉炎症和细胞凋亡。并且还导致 NF-κB 和 MAPKs 通路的表达增加。此外,硒缺乏显着增加TNF-α、IL-1β和IL-6以及促凋亡因子BAX、p53、caspase-7和caspase-3的表达,同时降低抗凋亡因子Bcl的表达-2 和 Bcl-xl。综上所述,缺硒降低了抗氧化酶的活性,导致ROS过度积累,引起氧化应激,影响鲤鱼的免疫功能,导致肌肉炎症和细胞凋亡。并且还导致 NF-κB 和 MAPKs 通路的表达增加。此外,硒缺乏显着增加TNF-α、IL-1β和IL-6以及促凋亡因子BAX、p53、caspase-7和caspase-3的表达,同时降低抗凋亡因子Bcl的表达-2 和 Bcl-xl。综上所述,缺硒降低了抗氧化酶的活性,导致ROS过度积累,引起氧化应激,影响鲤鱼的免疫功能,导致肌肉炎症和细胞凋亡。
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Selenium deficiency induced inflammation and apoptosis via NF-κB and MAPKs pathways in muscle of common carp (Cyprinus carpio L.)
Selenium (Se), one of the essential trace elements of fish, regulates immune system function and maintains immune homeostasis. Muscle is the important tissue that generate movement and maintain posture. At present, there are few studies on the effects of Se deficiency on carp muscle. In this experiment, carps were fed with dietary with different Se content to successfully establish a Se deficiency model. Low-Se dietary led to the decrease of Se content in muscle. Histological analysis showed that Se deficiency resulted in muscle fiber fragmentation, dissolution, disarrangement and increased myocyte apoptosis. Transcriptome revealed a total of 367 differentially expressed genes (DEGs) were screened, including 213 up-regulated DEGs and 154 down-regulated DEGs. Bioinformatics analysis showed that DEGs were concentrated in oxidation−reduction process, inflammation and apoptosis, and were related to NF-κB and MAPKs pathways. Further exploration of the mechanism showed that Se deficiency led to excessive accumulation of ROS, decreased the activity of antioxidant enzymes, and also resulted in increased expression of the NF-κB and MAPKs pathways. In addition, Se deficiency significantly increased the expressions of TNF-α, IL-1β and IL-6, and the pro-apoptotic factors BAX, p53, caspase-7 and caspase-3, while decreased the expressions of anti-apoptotic factors Bcl-2 and Bcl-xl. In conclusion, Se deficiency reduced the activities of antioxidant enzymes and led to excessive accumulation of ROS, which caused oxidative stress and affected the immune function of carp, leading to muscle inflammation and apoptosis.