摘要:
Selenium, as an essential trace element, exerts health effects that are contingent not only on the quantity consumed but also on the specific selenium species present in the dietary. The aim of this study was to investigate the effects of different selenium supplements on the distribution of selenium content, the forms of selenium, and its in vitro bioaccessibility in piglets. Inductively coupled plasma mass spectrometry and high-performance liquid chromatography (HPLC-ICP/MS) were applied to analyze the selenium content and its speciation in tissues and organs of piglets fed with three selenium supplements, sodium selenite (SS), selenium-enriched Cardamine hirsute (CH), and selenium-enriched yeast (SY). The bioaccessibility experiments on the livers of seleniumenriched piglets were conducted by simulating human gastrointestinal digestion. It was found that the kidney has the highest selenium content among the 12 examined organs. The efficacy of different selenium sources in improving the selenium content in piglets ranked in descending order, is as follows: SY, SS, and CH. The predominant form of selenium in the longissimus dorsi muscle is selenomethionine (SeMet), accompanied by smaller quantities of selenocysteine (SeCys) and methyl selenocysteine (MeSeCys). In contrast, the predominant selenium form in the liver is SeCys, along with SeMet and MeSeCys. Piglets fed with Se-enriched yeast exhibited a significant increase in the content and proportion of SeMet in both the longissimus dorsi muscle and liver. Additionally, different selenium species demonstrated varied G and GI bioaccessilities, with SeMet being the highest and SeCys the lowest.
作者机构:
[肖勘; 周墨涵; 秦旭; Yu X.; 刘玉兰; 陈少魁] Hubei Key Laboratory of Animal Nutrition and Feed Science, School of Animal Science and Nutritional Engineering, Wuhan Polytechnic University, Wuhan, 430023, China
通讯机构:
[Xiao, K.] H;Hubei Key Laboratory of Animal Nutrition and Feed Science, China
摘要:
<jats:p>Quercetin (Que) is a flavonol compound found in plants, which has a variety of biological activities. Necroptosis, a special form of programmed cell death, plays a vital role in the development of many gastrointestinal diseases. This study aimed to explore whether Que could attenuate the intestinal injury and barrier dysfunction of piglets after deoxynivalenol (DON) exposure through modulating the necroptosis signaling pathway. Firstly, twenty-four weaned piglets were used in a 2 × 2 factorial design and the main factors, including Que (basal diet or diet supplemented with 100 mg/kg Que) and DON exposure (control feed or feed contaminated with 4 mg/kg DON). After feeding for 21 d, piglets were killed for samples. Next, the intestinal porcine epithelial cell line (IPEC-1) was pretreated with or without Que (10 μmol/mL) in the presence or absence of a DON challenge (0.5 μg/mL). Dietary Que increased the body weight, average daily gain, and average daily feed intake (p < 0.05) through the trial. Que supplementation improved the villus height, and enhanced the intestinal barrier function (p < 0.05) indicated by the higher protein expression of occludin and claudin-1 (p < 0.05) in the jejunum of the weaned piglets after DON exposure. Dietary Que also down-regulated the protein abundance of total receptor interacting protein kinase 1 (t-RIP1), phosphorylated RIP1 (p-RIP1), p-RIP3, total mixed lineage kinase domain-like protein (t-MLKL), and p-MLKL (p < 0.05) in piglets after DON exposure. Moreover, Que pretreatment increased the cell viability and decreased the lactate dehydrogenase (LDH) activity (p < 0.05) in the supernatant of IPEC-1 cells after DON challenge. Que treatment also improved the epithelial barrier function indicated by a higher transepithelial electrical resistance (TEER) (p < 0.001), lower fluorescein isothiocyanate-labeled dextran (FD4) flux (p < 0.001), and better distribution of occludin and claudin-1 (p < 0.05) after DON challenge. Additionally, pretreatment with Que also inhibited the protein abundance of t-RIP1, p-RIP1, t-RIP3, p-RIP3, t-MLKL, and p-MLKL (p < 0.05) in IPEC-1 cells after DON challenge. In general, our data suggest that Que can ameliorate DON-induced intestinal injury and barrier dysfunction associated with suppressing the necroptosis signaling pathway.</jats:p>
摘要:
<jats:sec><jats:title>Scope</jats:title><jats:p>Mycotoxins co‐contamination of agricultural products poses a serious threat to human and animal health, especially hepatic dysfunction. Zearalenone (ZEN), deoxynivalenol (DON), and aflatoxin B1 (AFB1) are three commonly co‐occurring mycotoxins. This study is to determine whether lycopene (LYC) can alleviate hepatic toxicity induced by the co‐occurrence of ZEN, DON, and AFB1 in mice.</jats:p></jats:sec><jats:sec><jats:title>Methods and results</jats:title><jats:p>Eighty 6‐week‐old male ICR mice are divided into four groups: CON group (solvent control), LYC group (10 mgkg<jats:sup>−1</jats:sup> LYC), Co‐M group (10 mgkg<jats:sup>−1</jats:sup> ZEN + 1 mgkg<jats:sup>−1</jats:sup> DON + 0.5 mgkg<jats:sup>−1</jats:sup> AFB1), and LYC+Co‐M group (10 mgkg<jats:sup>−1</jats:sup> LYC + 10 mgkg<jats:sup>−1</jats:sup> ZEN + 1 mgkg<jats:sup>−1</jats:sup> DON + 0.5 mgkg<jats:sup>−1</jats:sup> AFB1). The results show that LYC can suppress the co‐occurrence of mycotoxin‐induced mitochondrial swelling and vacuolization accompanied by dysregulation of indices of mitochondrial dynamics (<jats:italic>Mitofusin 1 (Mfn1)</jats:italic>, <jats:italic>Mfn2</jats:italic>, Optic atrophy 1 (<jats:italic>Opa1)</jats:italic>, Dynamin‐related protein 1 (<jats:italic>Drp1)</jats:italic>, Fission 1 (<jats:italic>Fis1)</jats:italic> at the mRNA level; DRP1 and FIS1 at the protein level). LYC effectively inhibits co‐occurrence of mycotoxin‐induced activation of Cytochrome P450 2E1, and early fibrosis, as determined by staining with Masson's trichrome and α‐SMA protein.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>LYC successfully attenuates early hepatic fibrosis mainly through antioxidant activities and prevented mitochondrial injury.</jats:p></jats:sec>
摘要:
<jats:title>Abstract</jats:title><jats:sec>
<jats:title>Background</jats:title>
<jats:p>Necroptosis and pyroptosis are newly identified forms of programmed cell death, which play a vital role in development of many gastrointestinal disorders. Although plant polyphenols have been reported to protect intestinal health, it is still unclear whether there is a beneficial role of plant polyphenols in modulating necroptosis and pyroptosis in intestinal porcine epithelial cell line (IPEC-1) infected with enterotoxigenic <jats:italic>Escherichia coli</jats:italic> (ETEC) K88. This research was conducted to explore whether plant polyphenols including protocatechuic acid (PCA) and quercetin (Que), attenuated inflammation and injury of IPEC-1 caused by ETEC K88 through regulating necroptosis and pyroptosis signaling pathways.</jats:p>
</jats:sec><jats:sec>
<jats:title>Methods</jats:title>
<jats:p>IPEC-1 cells were treated with PCA (40 μmol/L) or Que (10 μmol/L) in the presence or absence of ETEC K88.</jats:p>
</jats:sec><jats:sec>
<jats:title>Results</jats:title>
<jats:p>PCA and Que decreased ETEC K88 adhesion and endotoxin level (<jats:italic>P</jats:italic> < 0.05) in cell supernatant. PCA and Que increased cell number (<jats:italic>P</jats:italic> < 0.001) and decreased lactate dehydrogenases (LDH) activity (<jats:italic>P</jats:italic> < 0.05) in cell supernatant after ETEC infection. PCA and Que improved transepithelial electrical resistance (TEER) (<jats:italic>P</jats:italic> < 0.001) and reduced fluorescein isothiocyanate-labeled dextran (FD4) flux (<jats:italic>P</jats:italic> < 0.001), and enhanced membrane protein abundance of occludin, claudin-1 and ZO-1 (<jats:italic>P</jats:italic> < 0.05), and rescued distribution of these tight junction proteins (<jats:italic>P</jats:italic> < 0.05) after ETEC infection. PCA and Que also declined cell necrosis ratio (<jats:italic>P</jats:italic> < 0.05). PCA and Que reduced mRNA abundance and concentration of tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-8 (<jats:italic>P</jats:italic> < 0.001), and down-regulated gene expression of toll-like receptors 4 (<jats:italic>TLR4</jats:italic>) and its downstream signals (<jats:italic>P</jats:italic> < 0.001) after ETEC infection. PCA and Que down-regulated protein abundance of total receptor interacting protein kinase 1 (t-RIP1), phosphorylated-RIP1 (p-RIP1), p-RIP1/t-RIP1, t-RIP3, p-RIP3, mixed lineage kinase domain-like protein (MLKL), p-MLKL, dynamin- related protein 1 (DRP1), phosphoglycerate mutase 5 (PGAM5) and high mobility group box1 (HMGB1) (<jats:italic>P</jats:italic> < 0.05) after ETEC infection. Moreover, PCA and Que reduced protein abundance of nod-like receptor protein 3 (NLRP3), nod-like receptors family CARD domain-containing protein 4 (NLRC4), apoptosis-associated speck-like protein containing a CARD (ASC), gasdermin D (GSDMD) and caspase-1 (<jats:italic>P</jats:italic> < 0.05) after ETEC infection.</jats:p>
</jats:sec><jats:sec>
<jats:title>Conclusions</jats:title>
<jats:p>In general, our data suggest that PCA and Que are capable of attenuating ETEC-caused intestinal inflammation and damage via inhibiting necroptosis and pyroptosis signaling pathways.</jats:p>
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