Selenium deficiency induced inflammation and apoptosis via NF-κB and MAPKs pathways in muscle of common carp (Cyprinus carpio L.)

Abstract

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.

Keywords: Apoptosis; Inflammation; Muscle; Oxidative stress; Se deficiency.