Selenium-Enriched Cardamine violifolia Alleviates LPS-Induced Hepatic Damage and Inflammation by Suppressing TLR4/NODs–Necroptosis Signal Axes in Piglets
Selenium-enriched Cardamine violifolia (SEC), a cruciferous plant, exerts excellent antioxidant and anti-inflammatory capacity, but its effect on hepatic function is unclear. This study investigated the effect and potential mechanism of SEC on hepatic injury induced by lipopolysaccharide (LPS). Twen...
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| Veröffentlicht in: | Biological trace element research 2024-02, Vol.202 (2), p.527-537 |
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| creator | Wang, Dan Xie, Wenshuai He, Wensheng Zhu, Huiling Zhang, Yue Gao, Qingyu Cong, Xin Cheng, Shuiyuan Liu, Yulan |
| description | Selenium-enriched
Cardamine violifolia
(SEC), a cruciferous plant, exerts excellent antioxidant and anti-inflammatory capacity, but its effect on hepatic function is unclear. This study investigated the effect and potential mechanism of SEC on hepatic injury induced by lipopolysaccharide (LPS). Twenty-four weaned piglets were randomly allotted to treatment with SEC (0.3 mg/kg Se) and/or LPS (100 μg/kg). After 28 days of the trial, pigs were injected with LPS to induce hepatic injury. These results indicated that SEC supplementation attenuated LPS-induced hepatic morphological injury and reduced aspartate aminotransferase (AST) and alkaline phosphatase (ALP) activities in plasma. SEC also inhibited the expression of pro-inflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-α) after the LPS challenge. In addition, SEC improved hepatic antioxidant capacity via enhancing glutathione peroxidase (GSH-Px) activity and decreasing malondialdehyde (MDA) concentration. Moreover, SEC downregulated the mRNA expression of hepatic myeloid differentiation factor 88 (MyD88) and nucleotide-binding oligomerization domain proteins 1 (NOD1) and its adaptor molecule receptor interacting protein kinase 2 (RIPK2). SEC also alleviated LPS-induced hepatic necroptosis by inhibiting RIPK1, RIPK3, and mixed-lineage kinase domain-like (MLKL) expression. These data suggest that SEC potentially mitigates LPS-induced hepatic injury via inhibiting Toll-like receptor 4 (TLR4)/NOD2 and necroptosis signaling pathways in weaned piglets. |
| doi_str_mv | 10.1007/s12011-023-03713-0 |
| format | Article |
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Cardamine violifolia
(SEC), a cruciferous plant, exerts excellent antioxidant and anti-inflammatory capacity, but its effect on hepatic function is unclear. This study investigated the effect and potential mechanism of SEC on hepatic injury induced by lipopolysaccharide (LPS). Twenty-four weaned piglets were randomly allotted to treatment with SEC (0.3 mg/kg Se) and/or LPS (100 μg/kg). After 28 days of the trial, pigs were injected with LPS to induce hepatic injury. These results indicated that SEC supplementation attenuated LPS-induced hepatic morphological injury and reduced aspartate aminotransferase (AST) and alkaline phosphatase (ALP) activities in plasma. SEC also inhibited the expression of pro-inflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-α) after the LPS challenge. In addition, SEC improved hepatic antioxidant capacity via enhancing glutathione peroxidase (GSH-Px) activity and decreasing malondialdehyde (MDA) concentration. Moreover, SEC downregulated the mRNA expression of hepatic myeloid differentiation factor 88 (MyD88) and nucleotide-binding oligomerization domain proteins 1 (NOD1) and its adaptor molecule receptor interacting protein kinase 2 (RIPK2). SEC also alleviated LPS-induced hepatic necroptosis by inhibiting RIPK1, RIPK3, and mixed-lineage kinase domain-like (MLKL) expression. These data suggest that SEC potentially mitigates LPS-induced hepatic injury via inhibiting Toll-like receptor 4 (TLR4)/NOD2 and necroptosis signaling pathways in weaned piglets.</description><identifier>ISSN: 0163-4984</identifier><identifier>EISSN: 1559-0720</identifier><identifier>DOI: 10.1007/s12011-023-03713-0</identifier><identifier>PMID: 37233925</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adaptor proteins ; Alkaline phosphatase ; Animals ; Antioxidants ; Antioxidants - pharmacology ; Aspartate aminotransferase ; Biochemistry ; Biomedical and Life Sciences ; Biotechnology ; Cardamine ; Cardamine - metabolism ; Cytokines ; Down-regulation ; Gene expression ; Glutathione ; Glutathione peroxidase ; Inflammation ; Inflammation - chemically induced ; Inflammation - drug therapy ; Injury prevention ; Interleukin 6 ; Kinases ; Life Sciences ; Lipopolysaccharides ; Liver ; Liver Diseases ; MAP kinase ; MyD88 protein ; Necroptosis ; Necrosis ; Nod1 protein ; NOD2 protein ; Nucleotides ; Nutrition ; Oligomerization ; Oncology ; Peroxidase ; Phosphatase ; Proteins ; Selenium ; Selenium - pharmacology ; Swine ; TLR4 protein ; Toll-Like Receptor 4 - metabolism ; Toll-like receptors ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>Biological trace element research, 2024-02, Vol.202 (2), p.527-537</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-5b27e4992f598838576de124b12e8be64a1d9077c2050bafd5a449049c86081a3</citedby><cites>FETCH-LOGICAL-c375t-5b27e4992f598838576de124b12e8be64a1d9077c2050bafd5a449049c86081a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12011-023-03713-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12011-023-03713-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37233925$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Dan</creatorcontrib><creatorcontrib>Xie, Wenshuai</creatorcontrib><creatorcontrib>He, Wensheng</creatorcontrib><creatorcontrib>Zhu, Huiling</creatorcontrib><creatorcontrib>Zhang, Yue</creatorcontrib><creatorcontrib>Gao, Qingyu</creatorcontrib><creatorcontrib>Cong, Xin</creatorcontrib><creatorcontrib>Cheng, Shuiyuan</creatorcontrib><creatorcontrib>Liu, Yulan</creatorcontrib><title>Selenium-Enriched Cardamine violifolia Alleviates LPS-Induced Hepatic Damage and Inflammation by Suppressing TLR4/NODs–Necroptosis Signal Axes in Piglets</title><title>Biological trace element research</title><addtitle>Biol Trace Elem Res</addtitle><addtitle>Biol Trace Elem Res</addtitle><description>Selenium-enriched
Cardamine violifolia
(SEC), a cruciferous plant, exerts excellent antioxidant and anti-inflammatory capacity, but its effect on hepatic function is unclear. This study investigated the effect and potential mechanism of SEC on hepatic injury induced by lipopolysaccharide (LPS). Twenty-four weaned piglets were randomly allotted to treatment with SEC (0.3 mg/kg Se) and/or LPS (100 μg/kg). After 28 days of the trial, pigs were injected with LPS to induce hepatic injury. These results indicated that SEC supplementation attenuated LPS-induced hepatic morphological injury and reduced aspartate aminotransferase (AST) and alkaline phosphatase (ALP) activities in plasma. SEC also inhibited the expression of pro-inflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-α) after the LPS challenge. In addition, SEC improved hepatic antioxidant capacity via enhancing glutathione peroxidase (GSH-Px) activity and decreasing malondialdehyde (MDA) concentration. Moreover, SEC downregulated the mRNA expression of hepatic myeloid differentiation factor 88 (MyD88) and nucleotide-binding oligomerization domain proteins 1 (NOD1) and its adaptor molecule receptor interacting protein kinase 2 (RIPK2). SEC also alleviated LPS-induced hepatic necroptosis by inhibiting RIPK1, RIPK3, and mixed-lineage kinase domain-like (MLKL) expression. These data suggest that SEC potentially mitigates LPS-induced hepatic injury via inhibiting Toll-like receptor 4 (TLR4)/NOD2 and necroptosis signaling pathways in weaned piglets.</description><subject>Adaptor proteins</subject><subject>Alkaline phosphatase</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Aspartate aminotransferase</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biotechnology</subject><subject>Cardamine</subject><subject>Cardamine - metabolism</subject><subject>Cytokines</subject><subject>Down-regulation</subject><subject>Gene expression</subject><subject>Glutathione</subject><subject>Glutathione peroxidase</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - drug therapy</subject><subject>Injury prevention</subject><subject>Interleukin 6</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Lipopolysaccharides</subject><subject>Liver</subject><subject>Liver Diseases</subject><subject>MAP kinase</subject><subject>MyD88 protein</subject><subject>Necroptosis</subject><subject>Necrosis</subject><subject>Nod1 protein</subject><subject>NOD2 protein</subject><subject>Nucleotides</subject><subject>Nutrition</subject><subject>Oligomerization</subject><subject>Oncology</subject><subject>Peroxidase</subject><subject>Phosphatase</subject><subject>Proteins</subject><subject>Selenium</subject><subject>Selenium - pharmacology</subject><subject>Swine</subject><subject>TLR4 protein</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>Toll-like receptors</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>0163-4984</issn><issn>1559-0720</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc9u1DAQhy0EotuFF-CALHHhEjr-k3V8XG0LXWnVVmw5R04yCa4cJ9hJRW-8A8e-HU-CyxaQOHDwWBp__o2tj5BXDN4xAHUSGQfGMuAiA6FYqk_IguW5zkBxeEoWwFYik7qQR-Q4xhsAprgWz8mRUFwIzfMFud-jQ2_nPjvzwdafsaEbExrTW4_01g7OtmkZunYOb62ZMNLd1T7b-mauE3uOo5lsTU9Nbzqkxjd061tn-j61B0-rO7qfxzFgjNZ39Hr3UZ5cXJ7GH9--X2AdhnEaoo10bztvHF1_TfHW0yvbOZziC_KsNS7iy8d9ST69P7venGe7yw_bzXqX1ULlU5ZXXKHUmre5LgpR5GrVIOOyYhyLClfSsEaDUjWHHCrTNrmRUoPUdbGCghmxJG8PuWMYvswYp7K3sUbnjMdhjiUvOIBgOpUlefMPejPMIb09URq0kDoNThQ_UOmHMQZsyzHY3oS7kkH5oK48qCuTuvKXuvIh-vVj9Fz12Py58ttVAsQBiOnIdxj-zv5P7E8M4KS4</recordid><startdate>20240201</startdate><enddate>20240201</enddate><creator>Wang, Dan</creator><creator>Xie, Wenshuai</creator><creator>He, Wensheng</creator><creator>Zhu, Huiling</creator><creator>Zhang, Yue</creator><creator>Gao, Qingyu</creator><creator>Cong, Xin</creator><creator>Cheng, Shuiyuan</creator><creator>Liu, Yulan</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QH</scope><scope>7QP</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>C1K</scope><scope>F1W</scope><scope>H97</scope><scope>K9.</scope><scope>L.G</scope><scope>7X8</scope></search><sort><creationdate>20240201</creationdate><title>Selenium-Enriched Cardamine violifolia Alleviates LPS-Induced Hepatic Damage and Inflammation by Suppressing TLR4/NODs–Necroptosis Signal Axes in Piglets</title><author>Wang, Dan ; 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Cardamine violifolia
(SEC), a cruciferous plant, exerts excellent antioxidant and anti-inflammatory capacity, but its effect on hepatic function is unclear. This study investigated the effect and potential mechanism of SEC on hepatic injury induced by lipopolysaccharide (LPS). Twenty-four weaned piglets were randomly allotted to treatment with SEC (0.3 mg/kg Se) and/or LPS (100 μg/kg). After 28 days of the trial, pigs were injected with LPS to induce hepatic injury. These results indicated that SEC supplementation attenuated LPS-induced hepatic morphological injury and reduced aspartate aminotransferase (AST) and alkaline phosphatase (ALP) activities in plasma. SEC also inhibited the expression of pro-inflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-α) after the LPS challenge. In addition, SEC improved hepatic antioxidant capacity via enhancing glutathione peroxidase (GSH-Px) activity and decreasing malondialdehyde (MDA) concentration. Moreover, SEC downregulated the mRNA expression of hepatic myeloid differentiation factor 88 (MyD88) and nucleotide-binding oligomerization domain proteins 1 (NOD1) and its adaptor molecule receptor interacting protein kinase 2 (RIPK2). SEC also alleviated LPS-induced hepatic necroptosis by inhibiting RIPK1, RIPK3, and mixed-lineage kinase domain-like (MLKL) expression. These data suggest that SEC potentially mitigates LPS-induced hepatic injury via inhibiting Toll-like receptor 4 (TLR4)/NOD2 and necroptosis signaling pathways in weaned piglets.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>37233925</pmid><doi>10.1007/s12011-023-03713-0</doi><tpages>11</tpages></addata></record> |
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| subjects | Adaptor proteins Alkaline phosphatase Animals Antioxidants Antioxidants - pharmacology Aspartate aminotransferase Biochemistry Biomedical and Life Sciences Biotechnology Cardamine Cardamine - metabolism Cytokines Down-regulation Gene expression Glutathione Glutathione peroxidase Inflammation Inflammation - chemically induced Inflammation - drug therapy Injury prevention Interleukin 6 Kinases Life Sciences Lipopolysaccharides Liver Liver Diseases MAP kinase MyD88 protein Necroptosis Necrosis Nod1 protein NOD2 protein Nucleotides Nutrition Oligomerization Oncology Peroxidase Phosphatase Proteins Selenium Selenium - pharmacology Swine TLR4 protein Toll-Like Receptor 4 - metabolism Toll-like receptors Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | Selenium-Enriched Cardamine violifolia Alleviates LPS-Induced Hepatic Damage and Inflammation by Suppressing TLR4/NODs–Necroptosis Signal Axes in Piglets |
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