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

Xu, Ran; Cao, Jing-wen; Xu, Tianchao; Liu, T; Zhu, Mengran; Guo, Mengyao

doi:10.1016/j.fsi.2023.108847

Cited by 22 publications

(4 citation statements)

References 42 publications

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“…Previous research has shown that inhibiting the p38 MAPK/NF-κB pathways can effectively decrease the transcription and expression levels of pro-inflammatory cytokines, leading to a reduction in inflammatory responses ( 16 , 70 ). In this study, we observed that the transcription levels of key regulatary elements (MAPK13, MAPK14 and NF-κB p65) were all notably reduced in the liver and intestine of largemouth bass fed with 0.60 and 1.20 g/Kg SePCH in comparison with the SePCH deficient groups, which is similar to earlier studies in grass carp ( 24 ), calve ( 12 ) and common carp ( C. carpio L) ( 71 ). Collectively, these results indicate that an adequate dietary SePCH can alleviate inflammatory responses by modulating the transcription levels of these pro- and anti-inflammatory genes (IL-1β, TNF-α, IFN-γ, IL-8, IL-12, TGF-β1 and IL-10) through inhibiting the p38 MAPK/NF-κB signaling transduction pathway and thus maintaining immune homeostasis in largemouth bass.…”

Section: Discussionsupporting

confidence: 90%

Effects of selenoprotein extracts from Cardamine hupingshanensis on growth, selenium metabolism, antioxidant capacity, immunity and intestinal health in largemouth bass Micropterus salmoides

Zhang,

Zhao,

Zhang

et al. 2024

Front. Immunol.

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This study aimed to assess the impact of dietary selenoprotein extracts from Cardamine hupingshanensis (SePCH) on the growth, hematological parameters, selenium metabolism, immune responses, antioxidant capacities, inflammatory reactions and intestinal barrier functions in juvenile largemouth bass (Micropterus salmoides). The base diet was supplemented with four different concentrations of SePCH: 0.00, 0.30, 0.60 and 1.20 g/Kg (actual selenium contents: 0.37, 0.59, 0.84 and 1.30 mg/kg). These concentrations were used to formulate four isonitrogenous and isoenergetic diets for juvenile largemouth bass during a 60-day culture period. Adequate dietary SePCH (0.60 and 1.20 g/Kg) significantly increased weight gain and daily growth rate compared to the control groups (0.00 g/Kg). Furthermore, 0.60 and 1.20 g/Kg SePCH significantly enhanced amounts of white blood cells, red blood cells, platelets, lymphocytes and monocytes, and levels of hemoglobin, mean corpuscular volume and mean corpuscular hemoglobin in the hemocytes. In addition, 0.60 and 1.20 g/Kg SePCH increased the mRNA expression levels of selenocysteine lyase, selenophosphate synthase 1, 15 kDa selenoprotein, selenoprotein T2, selenoprotein H, selenoprotein P and selenoprotein K in the fish liver and intestine compared to the controls. Adequate SePCH not only significantly elevated the activities of antioxidant enzymes (Total superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase), the levels of total antioxidant capacity and glutathione, while increased mRNA transcription levels of NF-E2-related factor 2, Cu/Zn-superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase. However, adequate SePCH significantly decreased levels of malondialdehyde and H2O2 and the mRNA expression levels of kelch-like ECH-associated protein 1a and kelch-like ECH-associated protein 1b in the fish liver and intestine compared to the controls. Meanwhile, adequate SePCH markedly enhanced the levels of immune factors (alkaline phosphatase, acid phosphatase, lysozyme, complement component 3, complement component 4 and immunoglobulin M) and innate immune-related genes (lysozyme, hepcidin, liver-expressed antimicrobial peptide 2, complement component 3 and complement component 4) in the fish liver and intestine compared to the controls. Adequate SePCH reduced the levels of pro-inflammatory cytokines (tumour necrosis factor-α, interleukin 8, interleukin 1β and interferon γ), while increasing transforming growth factor β1 levels at both transcriptional and protein levels in the liver and intestine. The mRNA expression levels of mitogen-activated protein kinase 13 (MAPK 13), MAPK14 and nuclear factor kappa B p65 were significantly reduced in the liver and intestine of fish fed with 0.60 and 1.20 g/Kg SePCH compared to the controls. Histological sections also demonstrated that 0.60 and 1.20 g/Kg SePCH significantly increased intestinal villus height and villus width compared to the controls. Furthermore, the mRNA expression levels of tight junction proteins (zonula occludens-1, zonula occludens-3, Claudin-1, Claudin-3, Claudin-5, Claudin-11, Claudin-23 and Claudin-34) and Mucin-17 were significantly upregulated in the intestinal epithelial cells of 0.60 and 1.20 g/Kg SePCH groups compared to the controls. In conclusion, these results found that 0.60 and 1.20 g/Kg dietary SePCH can not only improve growth, hematological parameters, selenium metabolism, antioxidant capacities, enhance immune responses and intestinal functions, but also alleviate inflammatory responses. This information can serve as a useful reference for formulating feeds for largemouth bass.

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Section: Discussionsupporting

confidence: 90%

Effects of selenoprotein extracts from Cardamine hupingshanensis on growth, selenium metabolism, antioxidant capacity, immunity and intestinal health in largemouth bass Micropterus salmoides

Zhang,

Zhao,

Zhang

et al. 2024

Front. Immunol.

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“…Se deficiency destroys the body's REDOX homeostasis, and ROS accumulation promotes the occurrence of oxidative stress in mastitis [37]. Previous studies have confirmed that Se deficiency causes inflammatory damage through oxidative stress in chickens [38], mice [39], carps [40], and cattle [41]. The present study established the Se-deficient MAC-T cell model in vitro by continuous delivery culture using FBS with very low Se concentrations.…”

Section: Discussionmentioning

confidence: 59%

Extracellular Vesicles Derived from Selenium-Deficient MAC-T Cells Aggravated Inflammation and Apoptosis by Triggering the Endoplasmic Reticulum (ER) Stress/PI3K-AKT-mTOR Pathway in Bovine Mammary Epithelial Cells

Chen,

Zhang,

Yang

et al. 2023

Antioxidants

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Selenium (Se) deficiency disrupts intracellular REDOX homeostasis and severely deteriorates immune and anti-inflammatory function in high-yielding periparturient dairy cattle. To investigate the damage of extracellular vesicles derived from Se-deficient MAC-T cells (SeD-EV) on normal mammary epithelial cells, an in vitro model of Se deficiency was established. Se-deficient MAC-T cells produced many ROS, promoting apoptosis and the release of inflammatory factors. Extracellular vesicles were successfully isolated by ultrahigh-speed centrifugation and identified by transmission electron microscopy, particle size analysis, and surface markers (CD63, CD81, HSP70, and TSG101). RNA sequencing was performed on exosomal RNA. A total of 9393 lncRNAs and 63,155 mRNAs transcripts were identified in the SeC and SeD groups, respectively, of which 126 lncRNAs and 955 mRNAs were differentially expressed. Furthermore, SeD-EV promoted apoptosis of normal MAC-T cells by TUNEL analysis. SeD-EV significantly inhibited Bcl-2, while Bax and Cleaved Caspase3 were greatly increased. Antioxidant capacity (CAT, T-AOC, SOD, and GSH-Px) was inhibited in SeD-EV-treated MAC-T cells. Additionally, p-PERK, p-eIF2α, ATF4, CHOP, and XBP1 were all elevated in MAC-T cells supplemented with SeD-EV. In addition, p-PI3K, p-Akt, and p-mTOR were decreased strikingly by SeD-EV. In conclusion, SeD-EV caused oxidative stress, thus triggering apoptosis and inflammation through endoplasmic reticulum stress and the PI3K-Akt-mTOR signaling pathway, which contributed to explaining the mechanism of Se deficiency causing mastitis.

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“…All of these in ammatory markers SOD, TNF and IL-6 had signi cant increased level among individuals administered with selenium [58]. Genes NF-kB, TNF and IL1B involved in in ammatory signaling pathway were found to had inverse association with selenium level as previous study shows the signi cantly increased level of mRNA expression of these genes through higher mRNA expression of toll like receptor (TLR4) with selenium de ciency [59]. However, other genes replicated through previous literature in present study including CBS and ITPR2 had decreased mRNA expression with selenium de ciency indicating direct correlation among activity of these genes and selenium availability.…”

Section: Discussionmentioning

confidence: 86%

Genetic Determinants of Selenium Availability, Selenium-Response, and Risk of Polycystic Ovary Syndrome

Sharma,

Khetarpal

2024

Biol Trace Elem Res

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Selenium is a trace element and its de ciency has been associated with the risk of PCOS, a multifactorial syndrome that affects a large number of women worldwide. Several databases and literature were searched to nd out genetic variants of the genes involved in selenium uptake, metabolism and regulation which may be signi cantly associated with risk of PCOS through Se related pathways. Genes whish require selenium for their biological actions to perform were also shortlisted. A total of eighteen signi cantly associated genes were identi ed which were shortlisted among forty-four variants that could play potential role in the PCOS risk among the study population. The genetic variant distribution data was available in-house and was obtained through GWAS study of the North India population. In silico tools were applied to understand the functional impact of these variants. Three variants namely LDLR(rs2228671), TNF (rs1041981), and SAA2 (rs2468844) are strongly associated with PCOS risk and have a functional impact on encoded protein. Certain variants of Se uptake genes such as DIO1, GPX2, TXNRD1, DIO2 GPX3 genes signi cantly increase or decrease risk of PCOS development. Se transporter gene SELENOP polymorphism rs9686343 with C allele signi cantly increased PCOS risk. Other potential genes that require selenium for their biological actions are involved in the in ammatory, antioxidant response, and energy homeostasis signaling pathways. Thus genetic variants of the population may affect the Se availability or Se de ciency may modulate the effect of Se-associated genes due to genetic polymorphism. This information may be helpful in dosage adjustment of Se supplementation for a population in order to have maximum bene ts.

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

Cited by 22 publications

References 42 publications

Effects of selenoprotein extracts from Cardamine hupingshanensis on growth, selenium metabolism, antioxidant capacity, immunity and intestinal health in largemouth bass Micropterus salmoides

Effects of selenoprotein extracts from Cardamine hupingshanensis on growth, selenium metabolism, antioxidant capacity, immunity and intestinal health in largemouth bass Micropterus salmoides

Extracellular Vesicles Derived from Selenium-Deficient MAC-T Cells Aggravated Inflammation and Apoptosis by Triggering the Endoplasmic Reticulum (ER) Stress/PI3K-AKT-mTOR Pathway in Bovine Mammary Epithelial Cells

Genetic Determinants of Selenium Availability, Selenium-Response, and Risk of Polycystic Ovary Syndrome

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