Luteolin Relieved DSS-Induced Colitis in Mice via HMGB1-TLR-NF-κB Signaling Pathway
The aim of this study was to investigate the effect of luteolin (Lu) on dextran sodium sulfate (DSS)–induced colitis in mice. Mice spleen was weighed. The length of colon was measured. H&E staining was used to observe the pathological changes of colon in mice. Superoxide dismutase (SOD) and malo...
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| Veröffentlicht in: | Inflammation 2021-04, Vol.44 (2), p.570-579 |
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| creator | Zuo, Ting Yue, Yinzi Wang, Xiaohui Li, Huan Yan, Shuai |
| description | The aim of this study was to investigate the effect of luteolin (Lu) on dextran sodium sulfate (DSS)–induced colitis in mice. Mice spleen was weighed. The length of colon was measured. H&E staining was used to observe the pathological changes of colon in mice. Superoxide dismutase (SOD) and malondialdehyde (MDA) in serum and intestine of mice were detected by commercial kits. Serum and intestinal cytokines were detected by ELISA kits. The expression of HMGB1 mRNA was detected by real-time PCR. The expression of HMGB1-TLR-NF-κB pathway was detected by Western blot. The level of HMGB1 was detected by immunohistochemistry. The results showed that Lu significantly increased the colon length/body weight ratio and significantly decreased the spleen weight/body weight ratio. Lu significantly increased serum and intestinal SOD levels and decreased MDA levels. Lu significantly increased serum and intestinal cytokine levels in mice. qPCR and immunohistochemistry results showed that Lu significantly reduced HMGB1 mRNA level and protein level. In addition, Lu significantly reduced the expression of HMGB1-TLR-NF-κB signaling pathway protein of intestine in mice. In conclusion, Lu significantly reduced and alleviated DSS-induced colitis in mice, and the mechanism was related to the regulation of intestinal HMGB1-TLR-NF-κB signaling pathway in mice. |
| doi_str_mv | 10.1007/s10753-020-01354-2 |
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Mice spleen was weighed. The length of colon was measured. H&E staining was used to observe the pathological changes of colon in mice. Superoxide dismutase (SOD) and malondialdehyde (MDA) in serum and intestine of mice were detected by commercial kits. Serum and intestinal cytokines were detected by ELISA kits. The expression of HMGB1 mRNA was detected by real-time PCR. The expression of HMGB1-TLR-NF-κB pathway was detected by Western blot. The level of HMGB1 was detected by immunohistochemistry. The results showed that Lu significantly increased the colon length/body weight ratio and significantly decreased the spleen weight/body weight ratio. Lu significantly increased serum and intestinal SOD levels and decreased MDA levels. Lu significantly increased serum and intestinal cytokine levels in mice. qPCR and immunohistochemistry results showed that Lu significantly reduced HMGB1 mRNA level and protein level. In addition, Lu significantly reduced the expression of HMGB1-TLR-NF-κB signaling pathway protein of intestine in mice. In conclusion, Lu significantly reduced and alleviated DSS-induced colitis in mice, and the mechanism was related to the regulation of intestinal HMGB1-TLR-NF-κB signaling pathway in mice.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-020-01354-2</identifier><identifier>PMID: 33015735</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Biomedical and Life Sciences ; Biomedicine ; Body weight ; Colitis ; Colon ; Cytokines ; Dextran ; Enzyme-linked immunosorbent assay ; Gene expression ; HMGB1 protein ; Immunohistochemistry ; Immunology ; Inflammatory bowel disease ; Internal Medicine ; Intestine ; Malondialdehyde ; mRNA ; NF-κB protein ; Original Article ; Pathology ; Pharmacology/Toxicology ; Rheumatology ; Signal transduction ; Sodium sulfate ; Spleen ; Superoxide dismutase</subject><ispartof>Inflammation, 2021-04, Vol.44 (2), p.570-579</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-14a59afc1b202fb7feec322d950f02ecffa7f9d54806c51f0ddd511da4aeb4a03</citedby><cites>FETCH-LOGICAL-c375t-14a59afc1b202fb7feec322d950f02ecffa7f9d54806c51f0ddd511da4aeb4a03</cites><orcidid>0000-0001-7175-0878</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10753-020-01354-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-020-01354-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33015735$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zuo, Ting</creatorcontrib><creatorcontrib>Yue, Yinzi</creatorcontrib><creatorcontrib>Wang, Xiaohui</creatorcontrib><creatorcontrib>Li, Huan</creatorcontrib><creatorcontrib>Yan, Shuai</creatorcontrib><title>Luteolin Relieved DSS-Induced Colitis in Mice via HMGB1-TLR-NF-κB Signaling Pathway</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>The aim of this study was to investigate the effect of luteolin (Lu) on dextran sodium sulfate (DSS)–induced colitis in mice. Mice spleen was weighed. The length of colon was measured. H&E staining was used to observe the pathological changes of colon in mice. Superoxide dismutase (SOD) and malondialdehyde (MDA) in serum and intestine of mice were detected by commercial kits. Serum and intestinal cytokines were detected by ELISA kits. The expression of HMGB1 mRNA was detected by real-time PCR. The expression of HMGB1-TLR-NF-κB pathway was detected by Western blot. The level of HMGB1 was detected by immunohistochemistry. The results showed that Lu significantly increased the colon length/body weight ratio and significantly decreased the spleen weight/body weight ratio. Lu significantly increased serum and intestinal SOD levels and decreased MDA levels. Lu significantly increased serum and intestinal cytokine levels in mice. qPCR and immunohistochemistry results showed that Lu significantly reduced HMGB1 mRNA level and protein level. In addition, Lu significantly reduced the expression of HMGB1-TLR-NF-κB signaling pathway protein of intestine in mice. In conclusion, Lu significantly reduced and alleviated DSS-induced colitis in mice, and the mechanism was related to the regulation of intestinal HMGB1-TLR-NF-κB signaling pathway in mice.</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Body weight</subject><subject>Colitis</subject><subject>Colon</subject><subject>Cytokines</subject><subject>Dextran</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Gene expression</subject><subject>HMGB1 protein</subject><subject>Immunohistochemistry</subject><subject>Immunology</subject><subject>Inflammatory bowel disease</subject><subject>Internal Medicine</subject><subject>Intestine</subject><subject>Malondialdehyde</subject><subject>mRNA</subject><subject>NF-κB protein</subject><subject>Original Article</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Rheumatology</subject><subject>Signal transduction</subject><subject>Sodium sulfate</subject><subject>Spleen</subject><subject>Superoxide dismutase</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp9kMlOwzAURS0EomX4ARYoEhs2hmc7jpslFAqVyqC2rC3XQ0mVJiVOivprfATfhEsZJBasnqV73n3WQeiIwBkBEOeegOAMAwUMhPEY0y3UJlwwTLlItlEbWAKYpalooT3vZwDQSTtsF7UYgzXH22g8aGpb5lkRDW2e2aU10dVohPuFaXR4d0NUZz4K-V2mbbTMVHR7d3NJ8HgwxPc9_P52GY2yaaFCxTR6VPXzq1odoB2ncm8Pv-Y-eupdj7u3ePBw0-9eDLBmgteYxIqnymkyoUDdRDhrNaPUpBwcUKudU8KlhscdSDQnDowxnBCjYmUnsQK2j043vYuqfGmsr-U889rmuSps2XhJ47iTsITGJKAnf9BZ2VTh24HiwDijIuWBohtKV6X3lXVyUWVzVa0kAbl2LjfOZXAuP51LGpaOv6qbydyan5VvyQFgG8CHqJja6vf2P7Uf6PuKwA</recordid><startdate>20210401</startdate><enddate>20210401</enddate><creator>Zuo, Ting</creator><creator>Yue, Yinzi</creator><creator>Wang, Xiaohui</creator><creator>Li, Huan</creator><creator>Yan, Shuai</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7175-0878</orcidid></search><sort><creationdate>20210401</creationdate><title>Luteolin Relieved DSS-Induced Colitis in Mice via HMGB1-TLR-NF-κB Signaling Pathway</title><author>Zuo, Ting ; Yue, Yinzi ; Wang, Xiaohui ; Li, Huan ; Yan, Shuai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-14a59afc1b202fb7feec322d950f02ecffa7f9d54806c51f0ddd511da4aeb4a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Body weight</topic><topic>Colitis</topic><topic>Colon</topic><topic>Cytokines</topic><topic>Dextran</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Gene expression</topic><topic>HMGB1 protein</topic><topic>Immunohistochemistry</topic><topic>Immunology</topic><topic>Inflammatory bowel disease</topic><topic>Internal Medicine</topic><topic>Intestine</topic><topic>Malondialdehyde</topic><topic>mRNA</topic><topic>NF-κB protein</topic><topic>Original Article</topic><topic>Pathology</topic><topic>Pharmacology/Toxicology</topic><topic>Rheumatology</topic><topic>Signal transduction</topic><topic>Sodium sulfate</topic><topic>Spleen</topic><topic>Superoxide dismutase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zuo, Ting</creatorcontrib><creatorcontrib>Yue, Yinzi</creatorcontrib><creatorcontrib>Wang, Xiaohui</creatorcontrib><creatorcontrib>Li, Huan</creatorcontrib><creatorcontrib>Yan, Shuai</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zuo, Ting</au><au>Yue, Yinzi</au><au>Wang, Xiaohui</au><au>Li, Huan</au><au>Yan, Shuai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Luteolin Relieved DSS-Induced Colitis in Mice via HMGB1-TLR-NF-κB Signaling Pathway</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2021-04-01</date><risdate>2021</risdate><volume>44</volume><issue>2</issue><spage>570</spage><epage>579</epage><pages>570-579</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><abstract>The aim of this study was to investigate the effect of luteolin (Lu) on dextran sodium sulfate (DSS)–induced colitis in mice. Mice spleen was weighed. The length of colon was measured. H&E staining was used to observe the pathological changes of colon in mice. Superoxide dismutase (SOD) and malondialdehyde (MDA) in serum and intestine of mice were detected by commercial kits. Serum and intestinal cytokines were detected by ELISA kits. The expression of HMGB1 mRNA was detected by real-time PCR. The expression of HMGB1-TLR-NF-κB pathway was detected by Western blot. The level of HMGB1 was detected by immunohistochemistry. The results showed that Lu significantly increased the colon length/body weight ratio and significantly decreased the spleen weight/body weight ratio. Lu significantly increased serum and intestinal SOD levels and decreased MDA levels. Lu significantly increased serum and intestinal cytokine levels in mice. qPCR and immunohistochemistry results showed that Lu significantly reduced HMGB1 mRNA level and protein level. In addition, Lu significantly reduced the expression of HMGB1-TLR-NF-κB signaling pathway protein of intestine in mice. In conclusion, Lu significantly reduced and alleviated DSS-induced colitis in mice, and the mechanism was related to the regulation of intestinal HMGB1-TLR-NF-κB signaling pathway in mice.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33015735</pmid><doi>10.1007/s10753-020-01354-2</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-7175-0878</orcidid></addata></record> |
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| subjects | Biomedical and Life Sciences Biomedicine Body weight Colitis Colon Cytokines Dextran Enzyme-linked immunosorbent assay Gene expression HMGB1 protein Immunohistochemistry Immunology Inflammatory bowel disease Internal Medicine Intestine Malondialdehyde mRNA NF-κB protein Original Article Pathology Pharmacology/Toxicology Rheumatology Signal transduction Sodium sulfate Spleen Superoxide dismutase |
| title | Luteolin Relieved DSS-Induced Colitis in Mice via HMGB1-TLR-NF-κB Signaling Pathway |
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