Chitosan oligosaccharides suppress LPS-induced IL-8 expression in human umbilical vein endothelial cells through blockade of p38 and Akt protein kinases
Aim： To investigate whether and how COS inhibited IL-8 production in LPS-induced human umbilical vein endothelial cells （HUVECs）. Methods： RT-PCR, enzyme-linked immunosorbent assays （ELISA） and Western blotting were used to study IL-8 expression and related signaling pathway. Wound healing migration...
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| Veröffentlicht in: | Acta pharmacologica Sinica 2011-04, Vol.32 (4), p.478-486 |
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| creator | Liu, Hong-tao Huang, Pei Ma, Pan Liu, Qi-shun Yu, Chao Du, Yu-guang |
| description | Aim： To investigate whether and how COS inhibited IL-8 production in LPS-induced human umbilical vein endothelial cells （HUVECs）. Methods： RT-PCR, enzyme-linked immunosorbent assays （ELISA） and Western blotting were used to study IL-8 expression and related signaling pathway. Wound healing migration assays and monocytic cell adhesion analysis were used to explore the chemotactic and adhesive activities of HUVECs. Results： COS 50-200 μg/mL exerted a significant inhibitory effect on LPS 100 ng/mL-induced IL-8 expression in HUVECs at both the transcriptional and translational levels. In addition, COS 50-200 μg/mL inhibited LPS-induced HUVEC migration and U937 monocyte adhesion to HUVECs in a concentration-dependent manner. Signal transduction studies suggest that COS blocked LPS-induced acti- vation of nuclear factor-κB （NF-κB） and activator protein-1 （AP-1） as well as phosphorylation of p38 mitogen-activated protein kinase （MAPK） and phosphokinase Akt. Further, the over-expression of LPS-induced IL-8 mRNA in HUVECs was suppressed by a p38 MAPK inhibitor （SB203580, 25 μmol/L） or a phosphatidylinositol 3-kinase （PI3K） inhibitor （LY294002, 50 pmol/L）. Conclusion： COS inhibited LPS-induced IL-8 expression in HUVECs through the blockade of the p38 MAPK and P13K/Akt signaling path-ways. |
| doi_str_mv | 10.1038/aps.2011.10 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4001981</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><cqvip_id>37863727</cqvip_id><sourcerecordid>860881672</sourcerecordid><originalsourceid>FETCH-LOGICAL-c470t-abaa75678a0baba4a2563700c65e59aaf727c5b07303a59cce531810450753d33</originalsourceid><addsrcrecordid>eNptkU2P0zAQhiMEYpfCiTsyXDhAlvFX7F6QVhUfK1UCCThbjuMm3iZ21k5W8E_4uTi0lA9x8oznmXc8foviMYYLDFS-0mO6IIBxzu4U51gwXgrC2d0cVwKXDCQ9Kx6kdA1ACcXr-8UZwaySINl58X3TuSkk7VHoXZsDYzodXWMTSvM4RpsS2n78VDrfzMY26GpbSmS__iy44JHzqJuH3D4Pteud0T26tfnS-iZMne1dvjC27xOauhjmtkN1H8xeNxaFHRqpRNo36HI_oTGGaencO6-TTQ-LezvdJ_voeK6KL2_ffN68L7cf3l1tLrelYQKmUtdaC14JqaHOMdOEV1QAmIpbvtZ6J4gwvAZBgWq-NsZyiiUGxkFw2lC6Kl4fdMe5HmxjrJ-i7tUY3aDjNxW0U39XvOtUG24VA8BribPA86NADDezTZMaXFpW1t6GOSlZgZTZCZLJZ_-Q12GOPm-3QAQTYJChFwfIxJBStLvTUzCoxW-V_VaL30u2Kp78-foT-8vgDLw8ACmXfGvj75n_13t6nN4F397kjpMkFTL_LBH0Bx1nwoE</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>860212040</pqid></control><display><type>article</type><title>Chitosan oligosaccharides suppress LPS-induced IL-8 expression in human umbilical vein endothelial cells through blockade of p38 and Akt protein kinases</title><source>MEDLINE</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>Free Full-Text Journals in Chemistry</source><creator>Liu, Hong-tao ; Huang, Pei ; Ma, Pan ; Liu, Qi-shun ; Yu, Chao ; Du, Yu-guang</creator><creatorcontrib>Liu, Hong-tao ; Huang, Pei ; Ma, Pan ; Liu, Qi-shun ; Yu, Chao ; Du, Yu-guang</creatorcontrib><description>Aim： To investigate whether and how COS inhibited IL-8 production in LPS-induced human umbilical vein endothelial cells （HUVECs）. Methods： RT-PCR, enzyme-linked immunosorbent assays （ELISA） and Western blotting were used to study IL-8 expression and related signaling pathway. Wound healing migration assays and monocytic cell adhesion analysis were used to explore the chemotactic and adhesive activities of HUVECs. Results： COS 50-200 μg/mL exerted a significant inhibitory effect on LPS 100 ng/mL-induced IL-8 expression in HUVECs at both the transcriptional and translational levels. In addition, COS 50-200 μg/mL inhibited LPS-induced HUVEC migration and U937 monocyte adhesion to HUVECs in a concentration-dependent manner. Signal transduction studies suggest that COS blocked LPS-induced acti- vation of nuclear factor-κB （NF-κB） and activator protein-1 （AP-1） as well as phosphorylation of p38 mitogen-activated protein kinase （MAPK） and phosphokinase Akt. Further, the over-expression of LPS-induced IL-8 mRNA in HUVECs was suppressed by a p38 MAPK inhibitor （SB203580, 25 μmol/L） or a phosphatidylinositol 3-kinase （PI3K） inhibitor （LY294002, 50 pmol/L）. Conclusion： COS inhibited LPS-induced IL-8 expression in HUVECs through the blockade of the p38 MAPK and P13K/Akt signaling path-ways.</description><identifier>ISSN: 1671-4083</identifier><identifier>EISSN: 1745-7254</identifier><identifier>DOI: 10.1038/aps.2011.10</identifier><identifier>PMID: 21468084</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Akt ; Base Sequence ; Biomedical and Life Sciences ; Biomedicine ; Cells, Cultured ; Chitosan - pharmacology ; DNA Primers ; Enzyme-Linked Immunosorbent Assay ; Humans ; Immunology ; Interleukin-8 - pharmacology ; Internal Medicine ; Lipopolysaccharides - pharmacology ; LPS ; Medical Microbiology ; Oligosaccharides - pharmacology ; Original ; original-article ; p38 Mitogen-Activated Protein Kinases - metabolism ; p38丝裂原活化蛋白激酶 ; Pharmacology/Toxicology ; Reverse Transcriptase Polymerase Chain Reaction ; Umbilical Veins - cytology ; Umbilical Veins - drug effects ; Umbilical Veins - enzymology ; Umbilical Veins - metabolism ; Vaccine ; Western印迹法 ; 人脐静脉内皮细胞 ; 封锁 ; 细胞表达 ; 诱导产生</subject><ispartof>Acta pharmacologica Sinica, 2011-04, Vol.32 (4), p.478-486</ispartof><rights>CPS and SIMM 2011</rights><rights>Copyright Nature Publishing Group Apr 2011</rights><rights>Copyright © 2011 CPS and SIMM 2011 CPS and SIMM</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-abaa75678a0baba4a2563700c65e59aaf727c5b07303a59cce531810450753d33</citedby><cites>FETCH-LOGICAL-c470t-abaa75678a0baba4a2563700c65e59aaf727c5b07303a59cce531810450753d33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/95561A/95561A.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4001981/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4001981/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21468084$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Hong-tao</creatorcontrib><creatorcontrib>Huang, Pei</creatorcontrib><creatorcontrib>Ma, Pan</creatorcontrib><creatorcontrib>Liu, Qi-shun</creatorcontrib><creatorcontrib>Yu, Chao</creatorcontrib><creatorcontrib>Du, Yu-guang</creatorcontrib><title>Chitosan oligosaccharides suppress LPS-induced IL-8 expression in human umbilical vein endothelial cells through blockade of p38 and Akt protein kinases</title><title>Acta pharmacologica Sinica</title><addtitle>Acta Pharmacol Sin</addtitle><addtitle>Acta Pharmacologica Sinica</addtitle><description>Aim： To investigate whether and how COS inhibited IL-8 production in LPS-induced human umbilical vein endothelial cells （HUVECs）. Methods： RT-PCR, enzyme-linked immunosorbent assays （ELISA） and Western blotting were used to study IL-8 expression and related signaling pathway. Wound healing migration assays and monocytic cell adhesion analysis were used to explore the chemotactic and adhesive activities of HUVECs. Results： COS 50-200 μg/mL exerted a significant inhibitory effect on LPS 100 ng/mL-induced IL-8 expression in HUVECs at both the transcriptional and translational levels. In addition, COS 50-200 μg/mL inhibited LPS-induced HUVEC migration and U937 monocyte adhesion to HUVECs in a concentration-dependent manner. Signal transduction studies suggest that COS blocked LPS-induced acti- vation of nuclear factor-κB （NF-κB） and activator protein-1 （AP-1） as well as phosphorylation of p38 mitogen-activated protein kinase （MAPK） and phosphokinase Akt. Further, the over-expression of LPS-induced IL-8 mRNA in HUVECs was suppressed by a p38 MAPK inhibitor （SB203580, 25 μmol/L） or a phosphatidylinositol 3-kinase （PI3K） inhibitor （LY294002, 50 pmol/L）. Conclusion： COS inhibited LPS-induced IL-8 expression in HUVECs through the blockade of the p38 MAPK and P13K/Akt signaling path-ways.</description><subject>Akt</subject><subject>Base Sequence</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cells, Cultured</subject><subject>Chitosan - pharmacology</subject><subject>DNA Primers</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Humans</subject><subject>Immunology</subject><subject>Interleukin-8 - pharmacology</subject><subject>Internal Medicine</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>LPS</subject><subject>Medical Microbiology</subject><subject>Oligosaccharides - pharmacology</subject><subject>Original</subject><subject>original-article</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>p38丝裂原活化蛋白激酶</subject><subject>Pharmacology/Toxicology</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Umbilical Veins - cytology</subject><subject>Umbilical Veins - drug effects</subject><subject>Umbilical Veins - enzymology</subject><subject>Umbilical Veins - metabolism</subject><subject>Vaccine</subject><subject>Western印迹法</subject><subject>人脐静脉内皮细胞</subject><subject>封锁</subject><subject>细胞表达</subject><subject>诱导产生</subject><issn>1671-4083</issn><issn>1745-7254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkU2P0zAQhiMEYpfCiTsyXDhAlvFX7F6QVhUfK1UCCThbjuMm3iZ21k5W8E_4uTi0lA9x8oznmXc8foviMYYLDFS-0mO6IIBxzu4U51gwXgrC2d0cVwKXDCQ9Kx6kdA1ACcXr-8UZwaySINl58X3TuSkk7VHoXZsDYzodXWMTSvM4RpsS2n78VDrfzMY26GpbSmS__iy44JHzqJuH3D4Pteud0T26tfnS-iZMne1dvjC27xOauhjmtkN1H8xeNxaFHRqpRNo36HI_oTGGaencO6-TTQ-LezvdJ_voeK6KL2_ffN68L7cf3l1tLrelYQKmUtdaC14JqaHOMdOEV1QAmIpbvtZ6J4gwvAZBgWq-NsZyiiUGxkFw2lC6Kl4fdMe5HmxjrJ-i7tUY3aDjNxW0U39XvOtUG24VA8BribPA86NADDezTZMaXFpW1t6GOSlZgZTZCZLJZ_-Q12GOPm-3QAQTYJChFwfIxJBStLvTUzCoxW-V_VaL30u2Kp78-foT-8vgDLw8ACmXfGvj75n_13t6nN4F397kjpMkFTL_LBH0Bx1nwoE</recordid><startdate>20110401</startdate><enddate>20110401</enddate><creator>Liu, Hong-tao</creator><creator>Huang, Pei</creator><creator>Ma, Pan</creator><creator>Liu, Qi-shun</creator><creator>Yu, Chao</creator><creator>Du, Yu-guang</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</scope><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>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20110401</creationdate><title>Chitosan oligosaccharides suppress LPS-induced IL-8 expression in human umbilical vein endothelial cells through blockade of p38 and Akt protein kinases</title><author>Liu, Hong-tao ; Huang, Pei ; Ma, Pan ; Liu, Qi-shun ; Yu, Chao ; Du, Yu-guang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-abaa75678a0baba4a2563700c65e59aaf727c5b07303a59cce531810450753d33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Akt</topic><topic>Base Sequence</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cells, Cultured</topic><topic>Chitosan - pharmacology</topic><topic>DNA Primers</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Humans</topic><topic>Immunology</topic><topic>Interleukin-8 - pharmacology</topic><topic>Internal Medicine</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>LPS</topic><topic>Medical Microbiology</topic><topic>Oligosaccharides - pharmacology</topic><topic>Original</topic><topic>original-article</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>p38丝裂原活化蛋白激酶</topic><topic>Pharmacology/Toxicology</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Umbilical Veins - cytology</topic><topic>Umbilical Veins - drug effects</topic><topic>Umbilical Veins - enzymology</topic><topic>Umbilical Veins - metabolism</topic><topic>Vaccine</topic><topic>Western印迹法</topic><topic>人脐静脉内皮细胞</topic><topic>封锁</topic><topic>细胞表达</topic><topic>诱导产生</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Hong-tao</creatorcontrib><creatorcontrib>Huang, Pei</creatorcontrib><creatorcontrib>Ma, Pan</creatorcontrib><creatorcontrib>Liu, Qi-shun</creatorcontrib><creatorcontrib>Yu, Chao</creatorcontrib><creatorcontrib>Du, Yu-guang</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-医药卫生</collection><collection>中文科技期刊数据库- 镜像站点</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences 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>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</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><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Acta pharmacologica Sinica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Hong-tao</au><au>Huang, Pei</au><au>Ma, Pan</au><au>Liu, Qi-shun</au><au>Yu, Chao</au><au>Du, Yu-guang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chitosan oligosaccharides suppress LPS-induced IL-8 expression in human umbilical vein endothelial cells through blockade of p38 and Akt protein kinases</atitle><jtitle>Acta pharmacologica Sinica</jtitle><stitle>Acta Pharmacol Sin</stitle><addtitle>Acta Pharmacologica Sinica</addtitle><date>2011-04-01</date><risdate>2011</risdate><volume>32</volume><issue>4</issue><spage>478</spage><epage>486</epage><pages>478-486</pages><issn>1671-4083</issn><eissn>1745-7254</eissn><abstract>Aim： To investigate whether and how COS inhibited IL-8 production in LPS-induced human umbilical vein endothelial cells （HUVECs）. Methods： RT-PCR, enzyme-linked immunosorbent assays （ELISA） and Western blotting were used to study IL-8 expression and related signaling pathway. Wound healing migration assays and monocytic cell adhesion analysis were used to explore the chemotactic and adhesive activities of HUVECs. Results： COS 50-200 μg/mL exerted a significant inhibitory effect on LPS 100 ng/mL-induced IL-8 expression in HUVECs at both the transcriptional and translational levels. In addition, COS 50-200 μg/mL inhibited LPS-induced HUVEC migration and U937 monocyte adhesion to HUVECs in a concentration-dependent manner. Signal transduction studies suggest that COS blocked LPS-induced acti- vation of nuclear factor-κB （NF-κB） and activator protein-1 （AP-1） as well as phosphorylation of p38 mitogen-activated protein kinase （MAPK） and phosphokinase Akt. Further, the over-expression of LPS-induced IL-8 mRNA in HUVECs was suppressed by a p38 MAPK inhibitor （SB203580, 25 μmol/L） or a phosphatidylinositol 3-kinase （PI3K） inhibitor （LY294002, 50 pmol/L）. Conclusion： COS inhibited LPS-induced IL-8 expression in HUVECs through the blockade of the p38 MAPK and P13K/Akt signaling path-ways.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>21468084</pmid><doi>10.1038/aps.2011.10</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Akt Base Sequence Biomedical and Life Sciences Biomedicine Cells, Cultured Chitosan - pharmacology DNA Primers Enzyme-Linked Immunosorbent Assay Humans Immunology Interleukin-8 - pharmacology Internal Medicine Lipopolysaccharides - pharmacology LPS Medical Microbiology Oligosaccharides - pharmacology Original original-article p38 Mitogen-Activated Protein Kinases - metabolism p38丝裂原活化蛋白激酶 Pharmacology/Toxicology Reverse Transcriptase Polymerase Chain Reaction Umbilical Veins - cytology Umbilical Veins - drug effects Umbilical Veins - enzymology Umbilical Veins - metabolism Vaccine Western印迹法 人脐静脉内皮细胞 封锁 细胞表达 诱导产生 |
| title | Chitosan oligosaccharides suppress LPS-induced IL-8 expression in human umbilical vein endothelial cells through blockade of p38 and Akt protein kinases |
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