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Guggulsterone Attenuated Lipopolysaccharide-Induced Inflammatory Responses in Mouse Inner Medullary Collecting Duct-3 Cells
Guggulsterone (GS) is a phytosterol that has been used to treat inflammatory diseases such as colitis, obesity, and thrombosis. Although many previous studies have examined activities of GS, the effect of GS on lipopolysaccharide (LPS)-induced inflammatory responses in mouse inner medullary collecti...
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Published in: | Inflammation 2016-02, Vol.39 (1), p.87-95 |
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container_title | Inflammation |
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creator | Kim, Dong-Goo Bae, Gi-Sang Jo, Il-Joo Choi, Sun-Bok Kim, Myoung-Jin Jeong, Jun-Hyeok Kang, Dae-Gil Lee, Ho-Sub Song, Ho-Joon Park, Sung-Joo |
description | Guggulsterone (GS) is a phytosterol that has been used to treat inflammatory diseases such as colitis, obesity, and thrombosis. Although many previous studies have examined activities of GS, the effect of GS on lipopolysaccharide (LPS)-induced inflammatory responses in mouse inner medullary collecting duct-3 (mIMCD-3) cells have not been examined. Therefore, here, we investigated the anti-inflammatory action of GS on mIMCD-3 cells exposed to LPS. LPS treatment on mIMCD-3 cells produced pro-inflammatory molecules such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) significantly; however, GS treatment significantly inhibited the production of pro-inflammatory molecules. In addition, GS inhibited the degradation of Iκ-Bα and translocation of NF-κB on mIMCD-3 cells. These results suggest that GS could inhibit inflammatory responses in collecting duct cells which could contribute to kidney injury during systemic infection. |
doi_str_mv | 10.1007/s10753-015-0226-x |
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Although many previous studies have examined activities of GS, the effect of GS on lipopolysaccharide (LPS)-induced inflammatory responses in mouse inner medullary collecting duct-3 (mIMCD-3) cells have not been examined. Therefore, here, we investigated the anti-inflammatory action of GS on mIMCD-3 cells exposed to LPS. LPS treatment on mIMCD-3 cells produced pro-inflammatory molecules such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) significantly; however, GS treatment significantly inhibited the production of pro-inflammatory molecules. In addition, GS inhibited the degradation of Iκ-Bα and translocation of NF-κB on mIMCD-3 cells. These results suggest that GS could inhibit inflammatory responses in collecting duct cells which could contribute to kidney injury during systemic infection.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-015-0226-x</identifier><identifier>PMID: 26260258</identifier><identifier>CODEN: INFLD4</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Acute Kidney Injury - drug therapy ; Animals ; Anti-Inflammatory Agents - pharmacology ; Biomedical and Life Sciences ; Biomedicine ; Cell Line ; Cyclooxygenase 2 - biosynthesis ; Female ; Immunology ; Inflammation - drug therapy ; Interleukin-6 - biosynthesis ; Internal Medicine ; Kidney Tubules, Collecting - cytology ; Kidney Tubules, Collecting - immunology ; Lipopolysaccharides ; Macrophages, Peritoneal - immunology ; Mice ; Mice, Inbred C57BL ; NF-KappaB Inhibitor alpha - metabolism ; Nitric Oxide Synthase Type II - biosynthesis ; Pathology ; Pharmacology/Toxicology ; Pregnenediones - pharmacology ; Reverse Transcriptase Polymerase Chain Reaction ; Rheumatology ; Toll-Like Receptor 4 - immunology ; Tumor Necrosis Factor-alpha - biosynthesis</subject><ispartof>Inflammation, 2016-02, Vol.39 (1), p.87-95</ispartof><rights>Springer Science+Business Media New York 2015</rights><rights>Springer Science+Business Media New York 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-e44ac65d19219c9fb3141e45e67b6d16c3909eea2ee79cfd72affa93c21163923</citedby><cites>FETCH-LOGICAL-c475t-e44ac65d19219c9fb3141e45e67b6d16c3909eea2ee79cfd72affa93c21163923</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26260258$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Dong-Goo</creatorcontrib><creatorcontrib>Bae, Gi-Sang</creatorcontrib><creatorcontrib>Jo, Il-Joo</creatorcontrib><creatorcontrib>Choi, Sun-Bok</creatorcontrib><creatorcontrib>Kim, Myoung-Jin</creatorcontrib><creatorcontrib>Jeong, Jun-Hyeok</creatorcontrib><creatorcontrib>Kang, Dae-Gil</creatorcontrib><creatorcontrib>Lee, Ho-Sub</creatorcontrib><creatorcontrib>Song, Ho-Joon</creatorcontrib><creatorcontrib>Park, Sung-Joo</creatorcontrib><title>Guggulsterone Attenuated Lipopolysaccharide-Induced Inflammatory Responses in Mouse Inner Medullary Collecting Duct-3 Cells</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>Guggulsterone (GS) is a phytosterol that has been used to treat inflammatory diseases such as colitis, obesity, and thrombosis. Although many previous studies have examined activities of GS, the effect of GS on lipopolysaccharide (LPS)-induced inflammatory responses in mouse inner medullary collecting duct-3 (mIMCD-3) cells have not been examined. Therefore, here, we investigated the anti-inflammatory action of GS on mIMCD-3 cells exposed to LPS. LPS treatment on mIMCD-3 cells produced pro-inflammatory molecules such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) significantly; however, GS treatment significantly inhibited the production of pro-inflammatory molecules. In addition, GS inhibited the degradation of Iκ-Bα and translocation of NF-κB on mIMCD-3 cells. These results suggest that GS could inhibit inflammatory responses in collecting duct cells which could contribute to kidney injury during systemic infection.</description><subject>Acute Kidney Injury - drug therapy</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Line</subject><subject>Cyclooxygenase 2 - biosynthesis</subject><subject>Female</subject><subject>Immunology</subject><subject>Inflammation - drug therapy</subject><subject>Interleukin-6 - biosynthesis</subject><subject>Internal Medicine</subject><subject>Kidney Tubules, Collecting - cytology</subject><subject>Kidney Tubules, Collecting - immunology</subject><subject>Lipopolysaccharides</subject><subject>Macrophages, Peritoneal - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NF-KappaB Inhibitor alpha - metabolism</subject><subject>Nitric Oxide Synthase Type II - biosynthesis</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Pregnenediones - pharmacology</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Rheumatology</subject><subject>Toll-Like Receptor 4 - immunology</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNqNkV1rFDEUhoNY7Lb6A7yRAW-8ieZjkkwuy9a2C1sKotchmzmzTskkYzKBFv98s2wVEQSvzsX7nPd8vAi9peQjJUR9ypQowTGhAhPGJH54gVZUKI6ZUPIlWhEuCeZaq1N0lvM9IaTTHX-FTplkkjDRrdDP67LfF58XSDFAc7EsEIpdoG-24xzn6B-zde67TWMPeBP64qq0CYO302SXmB6bL5DnGDLkZgzNbSwZqh4gNbfQF-9tRdbRe3DLGPbNZXEL5s0avM-v0clgfYY3z_Ucfbv6_HV9g7d315v1xRa7VokFQ9taJ0VPNaPa6WHHaUuhFSDVTvZUOq6JBrAMQGk39IrZYbCaO0ap5Jrxc_Th6Dun-KNAXsw0Zlc3sAHqvoYq2YlOkFb8Dyoorb-mFX3_F3ofSwr1kAPVdpwzrSpFj5RLMecEg5nTONWnGErMIURzDNHUEM0hRPNQe949O5fdBP3vjl-pVYAdgVylsIf0x-h_uj4BNYKozg</recordid><startdate>20160201</startdate><enddate>20160201</enddate><creator>Kim, Dong-Goo</creator><creator>Bae, Gi-Sang</creator><creator>Jo, Il-Joo</creator><creator>Choi, Sun-Bok</creator><creator>Kim, Myoung-Jin</creator><creator>Jeong, Jun-Hyeok</creator><creator>Kang, Dae-Gil</creator><creator>Lee, Ho-Sub</creator><creator>Song, Ho-Joon</creator><creator>Park, Sung-Joo</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>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>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20160201</creationdate><title>Guggulsterone Attenuated Lipopolysaccharide-Induced Inflammatory Responses in Mouse Inner Medullary Collecting Duct-3 Cells</title><author>Kim, Dong-Goo ; Bae, Gi-Sang ; Jo, Il-Joo ; Choi, Sun-Bok ; Kim, Myoung-Jin ; Jeong, Jun-Hyeok ; Kang, Dae-Gil ; Lee, Ho-Sub ; Song, Ho-Joon ; Park, Sung-Joo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-e44ac65d19219c9fb3141e45e67b6d16c3909eea2ee79cfd72affa93c21163923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Acute Kidney Injury - drug therapy</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Line</topic><topic>Cyclooxygenase 2 - biosynthesis</topic><topic>Female</topic><topic>Immunology</topic><topic>Inflammation - drug therapy</topic><topic>Interleukin-6 - biosynthesis</topic><topic>Internal Medicine</topic><topic>Kidney Tubules, Collecting - cytology</topic><topic>Kidney Tubules, Collecting - immunology</topic><topic>Lipopolysaccharides</topic><topic>Macrophages, Peritoneal - immunology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NF-KappaB Inhibitor alpha - metabolism</topic><topic>Nitric Oxide Synthase Type II - biosynthesis</topic><topic>Pathology</topic><topic>Pharmacology/Toxicology</topic><topic>Pregnenediones - pharmacology</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Rheumatology</topic><topic>Toll-Like Receptor 4 - immunology</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Dong-Goo</creatorcontrib><creatorcontrib>Bae, Gi-Sang</creatorcontrib><creatorcontrib>Jo, Il-Joo</creatorcontrib><creatorcontrib>Choi, Sun-Bok</creatorcontrib><creatorcontrib>Kim, Myoung-Jin</creatorcontrib><creatorcontrib>Jeong, Jun-Hyeok</creatorcontrib><creatorcontrib>Kang, Dae-Gil</creatorcontrib><creatorcontrib>Lee, Ho-Sub</creatorcontrib><creatorcontrib>Song, Ho-Joon</creatorcontrib><creatorcontrib>Park, Sung-Joo</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>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)</collection><collection>ProQuest Central</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>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Dong-Goo</au><au>Bae, Gi-Sang</au><au>Jo, Il-Joo</au><au>Choi, Sun-Bok</au><au>Kim, Myoung-Jin</au><au>Jeong, Jun-Hyeok</au><au>Kang, Dae-Gil</au><au>Lee, Ho-Sub</au><au>Song, Ho-Joon</au><au>Park, Sung-Joo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Guggulsterone Attenuated Lipopolysaccharide-Induced Inflammatory Responses in Mouse Inner Medullary Collecting Duct-3 Cells</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2016-02-01</date><risdate>2016</risdate><volume>39</volume><issue>1</issue><spage>87</spage><epage>95</epage><pages>87-95</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><coden>INFLD4</coden><abstract>Guggulsterone (GS) is a phytosterol that has been used to treat inflammatory diseases such as colitis, obesity, and thrombosis. Although many previous studies have examined activities of GS, the effect of GS on lipopolysaccharide (LPS)-induced inflammatory responses in mouse inner medullary collecting duct-3 (mIMCD-3) cells have not been examined. Therefore, here, we investigated the anti-inflammatory action of GS on mIMCD-3 cells exposed to LPS. LPS treatment on mIMCD-3 cells produced pro-inflammatory molecules such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) significantly; however, GS treatment significantly inhibited the production of pro-inflammatory molecules. In addition, GS inhibited the degradation of Iκ-Bα and translocation of NF-κB on mIMCD-3 cells. These results suggest that GS could inhibit inflammatory responses in collecting duct cells which could contribute to kidney injury during systemic infection.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>26260258</pmid><doi>10.1007/s10753-015-0226-x</doi><tpages>9</tpages></addata></record> |
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subjects | Acute Kidney Injury - drug therapy Animals Anti-Inflammatory Agents - pharmacology Biomedical and Life Sciences Biomedicine Cell Line Cyclooxygenase 2 - biosynthesis Female Immunology Inflammation - drug therapy Interleukin-6 - biosynthesis Internal Medicine Kidney Tubules, Collecting - cytology Kidney Tubules, Collecting - immunology Lipopolysaccharides Macrophages, Peritoneal - immunology Mice Mice, Inbred C57BL NF-KappaB Inhibitor alpha - metabolism Nitric Oxide Synthase Type II - biosynthesis Pathology Pharmacology/Toxicology Pregnenediones - pharmacology Reverse Transcriptase Polymerase Chain Reaction Rheumatology Toll-Like Receptor 4 - immunology Tumor Necrosis Factor-alpha - biosynthesis |
title | Guggulsterone Attenuated Lipopolysaccharide-Induced Inflammatory Responses in Mouse Inner Medullary Collecting Duct-3 Cells |
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