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Luteolin alleviates ulcerative colitis through SHP-1/STAT3 pathway
Background Previous studies have demonstrated that Luteolin has a positive effect on epithelial barrier integrity by promoting the function of tight protein, however, little is known about the underline mechanism of Luteolin. In this study, we constructed Caco-2 cell monolayer to explore the effects...
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| Published in: | Inflammation research 2021-06, Vol.70 (6), p.705-717 |
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| creator | Li, Bo-Lin Zhao, Dan-Yang Du, Peng-Li Wang, Xiao-Tian Yang, Qian Cai, Yan-Ru |
| description | Background
Previous studies have demonstrated that Luteolin has a positive effect on epithelial barrier integrity by promoting the function of tight protein, however, little is known about the underline mechanism of Luteolin. In this study, we constructed Caco-2 cell monolayer to explore the effects and the regulation mechanism of Luteolin in intestinal epithelial barrier integrity.
Methods
Caco-2 cells were co-treated with TNF-α, Interferon-γ (IFN-γ) and Luteolin for 24 h. Overexpression or knockdown of SHP-1 was applied to study the effects of protein phosphoserine phosphatase-1 (SHP-1) on epithelial barrier integrity. Cell viability was tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Barrier function was detected by trans-epithelial electrical resistance (TEER) and FITC-dextran assay. The expression levels of SHP-1, phosphorylation signal transducer and activator of transcription 3 (p-STAT3), STAT3 and tight junction proteins were measured by qRT-PCR or western blot. In vivo model of ulcerative colitis was established to detect the function of Luteolin in ulcerative colitis.
Results
We clarified that Luteolin protected intestinal epithelial barrier function of Caco-2 monolayers by increasing the resistance values and tight junction (TJ) protein expression. The expression of OCLN, CLDN1, and ZO1 was increased by Luteolin, while the expression of CLDN2 was decreased. Furthermore, Luteolin significantly alleviated the symptom of ulcerative colitis in DSS-induced mice. The in vitro cell model proved that overexpression of SHP-1 promotes the epithelial barrier function and knockdown of SHP-1 or STAT3 activation destroyed the protective effects of Luteolin on the expression of TJ proteins.
Conclusion
We found that the treatment of Luteolin promoted epithelial barrier function and Luteolin might preserve intestinal epithelial barrier function through suppression of STAT3 signaling pathway by SHP-1. |
| doi_str_mv | 10.1007/s00011-021-01468-9 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2537006521</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2537006521</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-b8268f0ad154a705035046e91708a45f4d731e27c0fee8e3a73cbb850c471e943</originalsourceid><addsrcrecordid>eNp9kF1LwzAUhoMobn78AS-k4HXcyVeTXs6hThgobIJ3Ie3SraNbZ5JO9u-NduqdF-EEzvO-Bx6ErgjcEgA58ABACAYaH-GpwtkR6hNOAWeg3o7jHyjDTDHooTPvVxFXVNFT1GM8BhgjfXQ3aYNt6mqTmLq2u8oE65O2LqwzodrZpIi7UPkkLF3TLpbJdPyCyWA6G85YsjVh-WH2F-ikNLW3l4d5jl4f7mejMZ48Pz6NhhNcMCkCzhVNVQlmTgQ3EgQwATy1GZGgDBcln0tGLJUFlNYqy4xkRZ4rAQWXxGacnaObrnfrmvfW-qBXTes28aSmgkmAVFASKdpRhWu8d7bUW1etjdtrAvpLm-606ahNf2vTWQxdH6rbfG3nv5EfTxFgHeDjarOw7u_2P7WfD_V14w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2537006521</pqid></control><display><type>article</type><title>Luteolin alleviates ulcerative colitis through SHP-1/STAT3 pathway</title><source>Springer Link</source><creator>Li, Bo-Lin ; Zhao, Dan-Yang ; Du, Peng-Li ; Wang, Xiao-Tian ; Yang, Qian ; Cai, Yan-Ru</creator><creatorcontrib>Li, Bo-Lin ; Zhao, Dan-Yang ; Du, Peng-Li ; Wang, Xiao-Tian ; Yang, Qian ; Cai, Yan-Ru</creatorcontrib><description>Background
Previous studies have demonstrated that Luteolin has a positive effect on epithelial barrier integrity by promoting the function of tight protein, however, little is known about the underline mechanism of Luteolin. In this study, we constructed Caco-2 cell monolayer to explore the effects and the regulation mechanism of Luteolin in intestinal epithelial barrier integrity.
Methods
Caco-2 cells were co-treated with TNF-α, Interferon-γ (IFN-γ) and Luteolin for 24 h. Overexpression or knockdown of SHP-1 was applied to study the effects of protein phosphoserine phosphatase-1 (SHP-1) on epithelial barrier integrity. Cell viability was tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Barrier function was detected by trans-epithelial electrical resistance (TEER) and FITC-dextran assay. The expression levels of SHP-1, phosphorylation signal transducer and activator of transcription 3 (p-STAT3), STAT3 and tight junction proteins were measured by qRT-PCR or western blot. In vivo model of ulcerative colitis was established to detect the function of Luteolin in ulcerative colitis.
Results
We clarified that Luteolin protected intestinal epithelial barrier function of Caco-2 monolayers by increasing the resistance values and tight junction (TJ) protein expression. The expression of OCLN, CLDN1, and ZO1 was increased by Luteolin, while the expression of CLDN2 was decreased. Furthermore, Luteolin significantly alleviated the symptom of ulcerative colitis in DSS-induced mice. The in vitro cell model proved that overexpression of SHP-1 promotes the epithelial barrier function and knockdown of SHP-1 or STAT3 activation destroyed the protective effects of Luteolin on the expression of TJ proteins.
Conclusion
We found that the treatment of Luteolin promoted epithelial barrier function and Luteolin might preserve intestinal epithelial barrier function through suppression of STAT3 signaling pathway by SHP-1.</description><identifier>ISSN: 1023-3830</identifier><identifier>EISSN: 1420-908X</identifier><identifier>DOI: 10.1007/s00011-021-01468-9</identifier><identifier>PMID: 34014331</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Allergology ; Animals ; Bile ; Biomedical and Life Sciences ; Biomedicine ; Caco-2 Cells ; Cell Membrane Permeability - drug effects ; Cell viability ; Colitis, Ulcerative - chemically induced ; Colitis, Ulcerative - drug therapy ; Colitis, Ulcerative - metabolism ; Colitis, Ulcerative - pathology ; Colon - drug effects ; Colon - metabolism ; Colon - pathology ; Dermatology ; Dextran ; Dextran Sulfate ; Dextrans ; Electrical resistivity ; Humans ; Immunology ; Inflammatory bowel disease ; Integrity ; Interferon ; Intestine ; Luteolin - pharmacology ; Luteolin - therapeutic use ; Male ; Mice ; Mice, Inbred C57BL ; Monolayers ; Neurology ; Original Research Paper ; Pharmacology/Toxicology ; Phosphorylation ; Phosphoserine ; Phosphoserine phosphatase ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 - genetics ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 - metabolism ; Proteins ; Rheumatology ; SHP-1 protein ; Signal transduction ; Signal Transduction - drug effects ; Stat3 protein ; STAT3 Transcription Factor - metabolism ; Tight Junction Proteins - genetics ; Tight Junction Proteins - metabolism ; Transcription ; Tumor necrosis factor-α ; Ulcerative colitis ; γ-Interferon</subject><ispartof>Inflammation research, 2021-06, Vol.70 (6), p.705-717</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Switzerland AG 2021</rights><rights>The Author(s), under exclusive licence to Springer Nature Switzerland AG 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-b8268f0ad154a705035046e91708a45f4d731e27c0fee8e3a73cbb850c471e943</citedby><cites>FETCH-LOGICAL-c375t-b8268f0ad154a705035046e91708a45f4d731e27c0fee8e3a73cbb850c471e943</cites><orcidid>0000-0002-2118-5468</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34014331$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Bo-Lin</creatorcontrib><creatorcontrib>Zhao, Dan-Yang</creatorcontrib><creatorcontrib>Du, Peng-Li</creatorcontrib><creatorcontrib>Wang, Xiao-Tian</creatorcontrib><creatorcontrib>Yang, Qian</creatorcontrib><creatorcontrib>Cai, Yan-Ru</creatorcontrib><title>Luteolin alleviates ulcerative colitis through SHP-1/STAT3 pathway</title><title>Inflammation research</title><addtitle>Inflamm. Res</addtitle><addtitle>Inflamm Res</addtitle><description>Background
Previous studies have demonstrated that Luteolin has a positive effect on epithelial barrier integrity by promoting the function of tight protein, however, little is known about the underline mechanism of Luteolin. In this study, we constructed Caco-2 cell monolayer to explore the effects and the regulation mechanism of Luteolin in intestinal epithelial barrier integrity.
Methods
Caco-2 cells were co-treated with TNF-α, Interferon-γ (IFN-γ) and Luteolin for 24 h. Overexpression or knockdown of SHP-1 was applied to study the effects of protein phosphoserine phosphatase-1 (SHP-1) on epithelial barrier integrity. Cell viability was tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Barrier function was detected by trans-epithelial electrical resistance (TEER) and FITC-dextran assay. The expression levels of SHP-1, phosphorylation signal transducer and activator of transcription 3 (p-STAT3), STAT3 and tight junction proteins were measured by qRT-PCR or western blot. In vivo model of ulcerative colitis was established to detect the function of Luteolin in ulcerative colitis.
Results
We clarified that Luteolin protected intestinal epithelial barrier function of Caco-2 monolayers by increasing the resistance values and tight junction (TJ) protein expression. The expression of OCLN, CLDN1, and ZO1 was increased by Luteolin, while the expression of CLDN2 was decreased. Furthermore, Luteolin significantly alleviated the symptom of ulcerative colitis in DSS-induced mice. The in vitro cell model proved that overexpression of SHP-1 promotes the epithelial barrier function and knockdown of SHP-1 or STAT3 activation destroyed the protective effects of Luteolin on the expression of TJ proteins.
Conclusion
We found that the treatment of Luteolin promoted epithelial barrier function and Luteolin might preserve intestinal epithelial barrier function through suppression of STAT3 signaling pathway by SHP-1.</description><subject>Allergology</subject><subject>Animals</subject><subject>Bile</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Caco-2 Cells</subject><subject>Cell Membrane Permeability - drug effects</subject><subject>Cell viability</subject><subject>Colitis, Ulcerative - chemically induced</subject><subject>Colitis, Ulcerative - drug therapy</subject><subject>Colitis, Ulcerative - metabolism</subject><subject>Colitis, Ulcerative - pathology</subject><subject>Colon - drug effects</subject><subject>Colon - metabolism</subject><subject>Colon - pathology</subject><subject>Dermatology</subject><subject>Dextran</subject><subject>Dextran Sulfate</subject><subject>Dextrans</subject><subject>Electrical resistivity</subject><subject>Humans</subject><subject>Immunology</subject><subject>Inflammatory bowel disease</subject><subject>Integrity</subject><subject>Interferon</subject><subject>Intestine</subject><subject>Luteolin - pharmacology</subject><subject>Luteolin - therapeutic use</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Monolayers</subject><subject>Neurology</subject><subject>Original Research Paper</subject><subject>Pharmacology/Toxicology</subject><subject>Phosphorylation</subject><subject>Phosphoserine</subject><subject>Phosphoserine phosphatase</subject><subject>Protein Tyrosine Phosphatase, Non-Receptor Type 6 - genetics</subject><subject>Protein Tyrosine Phosphatase, Non-Receptor Type 6 - metabolism</subject><subject>Proteins</subject><subject>Rheumatology</subject><subject>SHP-1 protein</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Stat3 protein</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Tight Junction Proteins - genetics</subject><subject>Tight Junction Proteins - metabolism</subject><subject>Transcription</subject><subject>Tumor necrosis factor-α</subject><subject>Ulcerative colitis</subject><subject>γ-Interferon</subject><issn>1023-3830</issn><issn>1420-908X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp9kF1LwzAUhoMobn78AS-k4HXcyVeTXs6hThgobIJ3Ie3SraNbZ5JO9u-NduqdF-EEzvO-Bx6ErgjcEgA58ABACAYaH-GpwtkR6hNOAWeg3o7jHyjDTDHooTPvVxFXVNFT1GM8BhgjfXQ3aYNt6mqTmLq2u8oE65O2LqwzodrZpIi7UPkkLF3TLpbJdPyCyWA6G85YsjVh-WH2F-ikNLW3l4d5jl4f7mejMZ48Pz6NhhNcMCkCzhVNVQlmTgQ3EgQwATy1GZGgDBcln0tGLJUFlNYqy4xkRZ4rAQWXxGacnaObrnfrmvfW-qBXTes28aSmgkmAVFASKdpRhWu8d7bUW1etjdtrAvpLm-606ahNf2vTWQxdH6rbfG3nv5EfTxFgHeDjarOw7u_2P7WfD_V14w</recordid><startdate>20210601</startdate><enddate>20210601</enddate><creator>Li, Bo-Lin</creator><creator>Zhao, Dan-Yang</creator><creator>Du, Peng-Li</creator><creator>Wang, Xiao-Tian</creator><creator>Yang, Qian</creator><creator>Cai, Yan-Ru</creator><general>Springer International Publishing</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>3V.</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><orcidid>https://orcid.org/0000-0002-2118-5468</orcidid></search><sort><creationdate>20210601</creationdate><title>Luteolin alleviates ulcerative colitis through SHP-1/STAT3 pathway</title><author>Li, Bo-Lin ; Zhao, Dan-Yang ; Du, Peng-Li ; Wang, Xiao-Tian ; Yang, Qian ; Cai, Yan-Ru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-b8268f0ad154a705035046e91708a45f4d731e27c0fee8e3a73cbb850c471e943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Allergology</topic><topic>Animals</topic><topic>Bile</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Caco-2 Cells</topic><topic>Cell Membrane Permeability - drug effects</topic><topic>Cell viability</topic><topic>Colitis, Ulcerative - chemically induced</topic><topic>Colitis, Ulcerative - drug therapy</topic><topic>Colitis, Ulcerative - metabolism</topic><topic>Colitis, Ulcerative - pathology</topic><topic>Colon - drug effects</topic><topic>Colon - metabolism</topic><topic>Colon - pathology</topic><topic>Dermatology</topic><topic>Dextran</topic><topic>Dextran Sulfate</topic><topic>Dextrans</topic><topic>Electrical resistivity</topic><topic>Humans</topic><topic>Immunology</topic><topic>Inflammatory bowel disease</topic><topic>Integrity</topic><topic>Interferon</topic><topic>Intestine</topic><topic>Luteolin - pharmacology</topic><topic>Luteolin - therapeutic use</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Monolayers</topic><topic>Neurology</topic><topic>Original Research Paper</topic><topic>Pharmacology/Toxicology</topic><topic>Phosphorylation</topic><topic>Phosphoserine</topic><topic>Phosphoserine phosphatase</topic><topic>Protein Tyrosine Phosphatase, Non-Receptor Type 6 - genetics</topic><topic>Protein Tyrosine Phosphatase, Non-Receptor Type 6 - metabolism</topic><topic>Proteins</topic><topic>Rheumatology</topic><topic>SHP-1 protein</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Stat3 protein</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Tight Junction Proteins - genetics</topic><topic>Tight Junction Proteins - metabolism</topic><topic>Transcription</topic><topic>Tumor necrosis factor-α</topic><topic>Ulcerative colitis</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Bo-Lin</creatorcontrib><creatorcontrib>Zhao, Dan-Yang</creatorcontrib><creatorcontrib>Du, Peng-Li</creatorcontrib><creatorcontrib>Wang, Xiao-Tian</creatorcontrib><creatorcontrib>Yang, Qian</creatorcontrib><creatorcontrib>Cai, Yan-Ru</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</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>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Inflammation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Bo-Lin</au><au>Zhao, Dan-Yang</au><au>Du, Peng-Li</au><au>Wang, Xiao-Tian</au><au>Yang, Qian</au><au>Cai, Yan-Ru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Luteolin alleviates ulcerative colitis through SHP-1/STAT3 pathway</atitle><jtitle>Inflammation research</jtitle><stitle>Inflamm. Res</stitle><addtitle>Inflamm Res</addtitle><date>2021-06-01</date><risdate>2021</risdate><volume>70</volume><issue>6</issue><spage>705</spage><epage>717</epage><pages>705-717</pages><issn>1023-3830</issn><eissn>1420-908X</eissn><abstract>Background
Previous studies have demonstrated that Luteolin has a positive effect on epithelial barrier integrity by promoting the function of tight protein, however, little is known about the underline mechanism of Luteolin. In this study, we constructed Caco-2 cell monolayer to explore the effects and the regulation mechanism of Luteolin in intestinal epithelial barrier integrity.
Methods
Caco-2 cells were co-treated with TNF-α, Interferon-γ (IFN-γ) and Luteolin for 24 h. Overexpression or knockdown of SHP-1 was applied to study the effects of protein phosphoserine phosphatase-1 (SHP-1) on epithelial barrier integrity. Cell viability was tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Barrier function was detected by trans-epithelial electrical resistance (TEER) and FITC-dextran assay. The expression levels of SHP-1, phosphorylation signal transducer and activator of transcription 3 (p-STAT3), STAT3 and tight junction proteins were measured by qRT-PCR or western blot. In vivo model of ulcerative colitis was established to detect the function of Luteolin in ulcerative colitis.
Results
We clarified that Luteolin protected intestinal epithelial barrier function of Caco-2 monolayers by increasing the resistance values and tight junction (TJ) protein expression. The expression of OCLN, CLDN1, and ZO1 was increased by Luteolin, while the expression of CLDN2 was decreased. Furthermore, Luteolin significantly alleviated the symptom of ulcerative colitis in DSS-induced mice. The in vitro cell model proved that overexpression of SHP-1 promotes the epithelial barrier function and knockdown of SHP-1 or STAT3 activation destroyed the protective effects of Luteolin on the expression of TJ proteins.
Conclusion
We found that the treatment of Luteolin promoted epithelial barrier function and Luteolin might preserve intestinal epithelial barrier function through suppression of STAT3 signaling pathway by SHP-1.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>34014331</pmid><doi>10.1007/s00011-021-01468-9</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-2118-5468</orcidid></addata></record> |
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| ispartof | Inflammation research, 2021-06, Vol.70 (6), p.705-717 |
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| subjects | Allergology Animals Bile Biomedical and Life Sciences Biomedicine Caco-2 Cells Cell Membrane Permeability - drug effects Cell viability Colitis, Ulcerative - chemically induced Colitis, Ulcerative - drug therapy Colitis, Ulcerative - metabolism Colitis, Ulcerative - pathology Colon - drug effects Colon - metabolism Colon - pathology Dermatology Dextran Dextran Sulfate Dextrans Electrical resistivity Humans Immunology Inflammatory bowel disease Integrity Interferon Intestine Luteolin - pharmacology Luteolin - therapeutic use Male Mice Mice, Inbred C57BL Monolayers Neurology Original Research Paper Pharmacology/Toxicology Phosphorylation Phosphoserine Phosphoserine phosphatase Protein Tyrosine Phosphatase, Non-Receptor Type 6 - genetics Protein Tyrosine Phosphatase, Non-Receptor Type 6 - metabolism Proteins Rheumatology SHP-1 protein Signal transduction Signal Transduction - drug effects Stat3 protein STAT3 Transcription Factor - metabolism Tight Junction Proteins - genetics Tight Junction Proteins - metabolism Transcription Tumor necrosis factor-α Ulcerative colitis γ-Interferon |
| title | Luteolin alleviates ulcerative colitis through SHP-1/STAT3 pathway |
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