The previous study indicated that transport stress resulted in oxidative damage and autophagy/mitophagy elevation, companied by NOX1 over- expression in the jejunal tissues of pigs. However, the transportation-related gene expression profile and NOX1 function in intestine remain to be explicated. In the current study, differentially expressed genes involved in PI3K-Akt and NF-κB pathways, oxidative stress and autophagy process have been identified in pig jejunal tissues after transcriptome analysis following transportation. The physiological functions of NOX1 down-regulation were explored against oxidative damage and excessive autophagy in porcine intestinal epithelial cells (IPEC-1) following NOX1 inhibitor ML171 and H2O2 treatments. NOX1 down-regulation could decrease the content of Malondialdehyde (MDA), Lactic dehydrogenase (LDH) activity and reactive oxygen species (ROS) level, and up-regulate superoxide dismutase (SOD) activity. Furthermore, mitochondrial membrane potential and content were restored, and the expressions of tight junction proteins (Claudin-1 and ZO-1) were also increased. Additionally, NOX1 inhibitior could down-regulate the expression of autophagy-associated proteins (ATG5, LC3, p62), accompanied by activating SIRT1/PGC-1α pathway. NOX1 down-regulation might alleviate oxidative stress-induced mitochondria damage and intestinal mucosal injury via modulating excessive autophagy and SIRT1/PGC-1α signaling pathway. The data will shed light on the molecular mechanism of NOX1 on intestine oxidative damage following pig transportation.
Keywords: Autophagy; NOX1; Oxidative damage; RNA-seq; Transport stress.
Copyright © 2020 Elsevier B.V. All rights reserved.