Selenium Deficiency Induces Inflammatory Response and Decreased Antimicrobial Peptide Expression in Chicken Jejunum Through Oxidative Stress.

Selenium deficiency can affect the level of selenoprotein in organs and tissues and cause inflammation. However, the mechanism of selenium deficiency on jejunal injury in chickens remains unclear. In this study, we established a selenium deficiency model in chickens by feeding a low selenium diet and observed ultrastructural and pathological changes in the jejunum. The expression levels of 25 selenoproteins, the levels of oxidative stress, tight junction (TJ) proteins, and antimicrobial peptides (AMP), as well as the expression levels of factors related to inflammatory signaling pathways, were examined in the intestine and analyzed using principal component analysis (PCA). The results of PCA and quantitative real-time PCR (qRT-PCR) showed that selenium deficiency mainly affected the expression of antioxidant selenoproteins in chicken jejunum, especially glutathione peroxidases, thioredoxin reductase, and iodothyronine deiodinase, thus weakening the antioxidant function in the intestine and inducing oxidative stress. We also found disruption of intestinal TJ structures, a significant reduction in TJ protein expression, and downregulation of antimicrobial peptide levels, suggesting that selenium deficiency led to damage of the intestinal barrier. In addition, a significant increase in inflammatory cell infiltration and expression of inflammatory factors was observed in the jejunum, indicating that selenium deficiency induces inflammatory injury. In conclusion, selenium deficiency downregulates antioxidant selenoproteins levels, induces oxidative stress, decreases intestinal AMP levels, and leads to inflammatory injury and disruption of the intestinal barrier in the jejunum. These results shed new light on the molecular mechanisms of intestinal damage caused by selenium deficiency.

Protective Effects of Astilbin Against Cadmium-Induced Apoptosis in Chicken Kidneys via Endoplasmic Reticulum Stress Signaling Pathway.

Cadmium (Cd) can cause endoplasmic reticulum stress (ERS) and apoptosis in animals. The kidney is an organ seriously affected by Cd because it can accumulate metal ions. Astilbin (ASB) is a dihydroflavonol rhamnoside, which has an anti-renal injury effect. This study aimed to evaluate the protective effect of ASB on Cd-induced ERS and apoptosis in the chicken kidney. In this study, a total of 120 1-day-old chickens were randomly divided into 4 groups. Chickens were fed with a basic diet (Con group), ASB 40 mg/kg (ASB group), CdCl2 150 mg/kg + ASB 40 mg/kg (ASB/Cd group), and CdCl2 150 mg/kg (Cd group) for 90 days. The results showed that Cd exposure induced pathological and ultrastructural damages and apoptosis in chicken kidneys. Compared with the Con group, metallothionein (MT1/MT2) level, nitric oxide (NO) content, inducible nitric oxide synthase (iNOS) activity, ERS-related genes 78-kDa glucose-regulated protein (Grp78), protein kinase PKR-like endoplasmic reticulum kinase (Perk), activating transcription factor 4 (Atf4) and CAAT/enhancer-binding protein (C/EBP) homologous protein (Chop), and pro-apoptotic gene B-cell lymphoma 2 (Bcl-2)-associated X (Bax), caspase-12, caspase-9, caspase-3 expression levels, and apoptotic rate were significantly increased in the Cd group. The expression level of Bcl-2 was significantly decreased in the Cd group. ASB/Cd combined treatment significantly improves the damage of chicken kidneys by ameliorating Cd-induced kidney ERS and apoptosis. Cd can cause the disorder of the GRP78 signal axis, activate the PERK-ATF4-CHOP pathway, aggravate the structural damage and dysfunction of ER, and promote the apoptosis of chicken kidneys, while the above changes were significantly alleviated in the ASB/Cd group. The results showed that ASB antagonizes the negative effects of Cd and against Cd-induced apoptosis in chicken kidneys via ERS signaling pathway.

LncRNA 0003250 accelerates heart autophagy and binds to miR-17-5p as a competitive endogenous RNA in chicken induced by selenium deficiency.

Long noncoding RNAs (LncRNAs) have been demonstrated to be associated with a variety of myocardial diseases, but how LncRNAs regulate autophagy in selenium (Se)-deficient myocardial injury is infrequently reported. Here, we screened out a novel long noncoding RNA, microRNA, and ATG7 through transcriptomic results. We employed a Se-deficient chicken model in vivo, and primary cultured cardiomyocytes treated by correlation in vitro. The results showed that Se deficiency upregulated the expression of ATG7, and miR-17-5p inhibited cardiomyocyte autophagy by targeting ATG7. Furthermore, we found that LncRNA 0003250 regulated miR-17-5p, and thus affected the expression of ATG7 and autophagic cell death. Our present study proposed a novel model for the regulation of cardiomyocytes autophagy, which includes LncRNA 0003250, miR-17-5p and ATG7 in the chicken heart. Our conclusions may provide a feasible diagnostic tool for Se-deficient cardiomyocyte injury.

chTLR4 pathway activation by Astragalus polysaccharide in bursa of Fabricius.

BACKGROUND: The Toll-like receptor 4 (TLR4) pathway involves in the pathogen recognition and defense against infection in mammals. Considering that avian and mammalian TLR are differentially mediated, the action of a natural product on avian TLR4 pathway was unclear. High, medium and low doses of Astragalus polysaccharide (APS), were treated the chicken at 7-days-old age by gavage. The sIgA level in the intestinal fluid, the expression of chTLR4 mRNA/protein in bursa of Fabricius as well as the expression of downstream molecules of chTLR4 (chMyD88, chTRIF, chNF-κB, chIRF3, chIFN-ß and chTNF-α) were measured on alternate days. RESULTS: The content of sIgA and the chTLR4 mRNA expression/protein level were increased in non-dose-dependent manner after APS supplement. Also, the expressions of a subset of MyD88-independent pathway genes were more than MyD88-independent, in particular with low doses of APS supplement for 7 days. CONCLUSIONS: These suggest that administration of APS activates chTLR4 pathway in bursa of Fabricius in MyD88-independent pathway. Meanwhile, low dose of APS shows better performance regarding the activation of chTLR4 and regulation of MyD88-independent pathway.