Roles of spermine in modulating the antioxidant status and Nrf2 signalling molecules expression in the thymus and spleen of suckling piglets—new insight

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The suckling period is known as a crucial phase of growth and development that mammals naturally experience. In commercial pig production, the suckling piglet is generally weaned early to obtain excellent economic profit. At this time, multiple biological stress responses are caused by early weaning, and weaning stress is highly prominent (Wang, Zeng, et al., 2016). Weaning stress can contribute to numerous biological processes, including enhanced disease susceptibility and metabolic disorders (Yin et al., 2013, 2014), impaired intestinal histomorphology and functions (Xiong et al., 2015, 2016; Zhu, Zhao, Chen, & Xu, 2012), reduced feed intake and suppressed growth (Campbell, Crenshaw, & Polo, 2013). Furthermore, weaning stress also exerts affirmative effects on generating excessive reactive oxygen species (ROS) in a normal amount of the body (Yin et al., 2014), which may further lead to oxidative stress and changes in many antioxidant enzymes in the antioxidant defence systems, such as superoxide dismutase, catalase and glutathione peroxidase (Han, Shuvaev, & Muzykantov, 2011). Suitable therapies and nutritional support (e.g., L‐arginine, N‐carbamylglutamate and putrescine) can provide beneficial effects to optimise weaning transition by mitigating the problems associated with early weaning (Wang, Li, et al., 2015; Wu et al., 2010).
It is well known that weaning induces an increase in the content of spermine in the intestinal mucosal of piglet (Wang, Tan, et al., 2016), implying that spermine has the important biological effects in animals. Spermine, known as polyamine, is a low‐molecular‐weight molecule ubiquitous in all living tissues and cells of mammals and non‐mammals (Polticelli, Salvi, Mariottini, Amendola, & Cervelli, 2012). In the literature, spermine has been implicated in diverse biological and physiological events, such as in regulating replication, transcription, translation and post‐translational modification (Mandala, Mandal, Johansson, Orjalo, & Hee Park, 2013); controlling protein synthesis and cell membrane transporter (Igarashi & Kashiwagi, 2010); modulating ion channel activities (Pegg, 2014); interacting with intracellular messengers (Igarashi & Kashiwagi, 2010); changing intestinal morphology (Fang, Jia, et al., 2016); and promoting immune response (Pegg, 2014). Spermine can also change systemic metabolic processes of the body through affecting lipid metabolism, energy metabolism, amino acid metabolism, cell membrane metabolism and gut microbiota metabolism (Liu, Fang, Yan, Jia, Zhao, Chen, et al., 2014, Liu, Fang, Yan, Jia, Zhao, Huang et al., 2014, Liu et al., 2015). Supplementation with spermine in breast milk can accelerate the early presence of splenic B cells in suckling rats (Pérez‐Cano, González‐Castro, Castellote, Franch, & Castell, 2010), but the effect of spermine intake on the spleen and thymus of pigs remains unknown. Spermine supplementation and extended spermine administration can improve the antioxidant capacity of the jejunum in suckling rats by enhancing free radical scavenging ability (Cao et al., 2015). Pigs can function as appropriate models for human studies because they are similar to humans than rats in terms of anatomy, neurobiology, cardiovascular systems, gastrointestinal tract, metabolic features and genome (Fan & Lai, 2013). However, no study has indicated the effects of spermine intake and its extended duration on the antioxidant status of the thymus and spleen in pigs. Currently, spermine and prolonged spermine ingestion focus on the changes in antioxidant enzymes in suckling animals (Cao et al., 2015; Fang, Liu, et al., 2016). Nevertheless, the relationship between spermine intake and its extended duration and antioxidant enzyme gene expression remains largely unclear. Previous studies showed that the expression levels of endogenous antioxidant enzyme genes are usually regulated by transcription factor nuclear factor erythroid 2‐related factor 2 (Nrf2) (Kensler, Wakabayashi, & Biswal, 2007; Zhang et al., 2013).
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