Protective effects of Schisandrin B on cigarette smoke-induced airway injury in mice through Nrf2 pathway
Schisandrin B (SchB), a dibenzocyclooctadiene derivative isolated from Schisandra chinensis, has been reported to have anti-inflammatory effects. However, the protective effects of SchB on cigarette smoke (CS)-induced lung inflammation remain unclear. This study was to investigate the effects of Sch...
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| Veröffentlicht in: | International immunopharmacology 2017-12, Vol.53, p.11-16 |
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| creator | Jia, Ruichun Zhang, Haogang Yang, Zhiping Zhao, Hong Liu, Fei Wang, Hui Miao, Meijuan Wang, Qiushi Liu, Yanhong |
| description | Schisandrin B (SchB), a dibenzocyclooctadiene derivative isolated from Schisandra chinensis, has been reported to have anti-inflammatory effects. However, the protective effects of SchB on cigarette smoke (CS)-induced lung inflammation remain unclear. This study was to investigate the effects of SchB on CS-induced lung inflammation in mice. The mice were exposed to CS to develop lung inflammation. SchB was given 1h before CS exposure daily for five consecutive days. The levels of inflammatory mediators TNF-α, IL-1β, and IL-6 in bronchoalveolar lavage fluid (BALF) were measured in this study. SOD, GSH, MPO and MDA contents were also detected. Furthermore, the expression of Nrf-2 and NF-κB were detected by western blot analysis. Histopathological analyses showed that SchB had protective effects against CS-induced lung inflammation. The levels of inflammatory mediators TNF-α, IL-1β, and IL-6 in BALF were also inhibited by SchB. CS-induced MPO activity and MDA content were inhibited by SchB. The levels of SOD and GSH were up-regulated by SchB. SchB significantly inhibited CS-induced NF-κB activation and up-regulated the expression of Nrf2 and HO-1. In conclusion, these data suggest that SchB protects against CS-induced lung inflammation by activating Nrf2 and inhibiting NF-κB signaling pathway.
•SchB had protective effects against CS-induced lung inflammation.•The levels of TNF-α and IL-1β in BALF were also inhibited by SchB.•The levels of SOD and GSH were up-regulated by SchB.•SchB significantly inhibited CS-induced NF-κB activation and up-regulated the expression of Nrf2 and HO-1. |
| doi_str_mv | 10.1016/j.intimp.2017.09.030 |
| format | Article |
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•SchB had protective effects against CS-induced lung inflammation.•The levels of TNF-α and IL-1β in BALF were also inhibited by SchB.•The levels of SOD and GSH were up-regulated by SchB.•SchB significantly inhibited CS-induced NF-κB activation and up-regulated the expression of Nrf2 and HO-1.</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2017.09.030</identifier><identifier>PMID: 29031142</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Alveoli ; Animals ; Anti-Inflammatory Agents - therapeutic use ; Bronchus ; Cells, Cultured ; Cigarette smoke ; Cigarette Smoking - adverse effects ; Cigarettes ; Cyclooctanes - therapeutic use ; Cytokines - metabolism ; Effects ; GA-binding protein ; Inflammation ; Interleukin 6 ; Lignans - therapeutic use ; Lung - drug effects ; Lung - pathology ; Lung diseases ; Lung inflammation ; Lungs ; Male ; Mice ; Mice, Inbred C57BL ; NF-E2-Related Factor 2 - metabolism ; NF-kappa B - metabolism ; NF-κB ; NF-κB protein ; Nrf-2 ; Pneumonia - chemically induced ; Pneumonia - drug therapy ; Polycyclic Compounds - therapeutic use ; Respiratory tract ; Schisandra - immunology ; Schisandrin B ; Signal Transduction ; Signaling ; Smoke ; Smoking ; Tumor necrosis factor-α</subject><ispartof>International immunopharmacology, 2017-12, Vol.53, p.11-16</ispartof><rights>2017</rights><rights>Copyright © 2017. Published by Elsevier B.V.</rights><rights>Copyright Elsevier BV Dec 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-a8bfdf67e90856eb4496f5f0557eb71f21dfe12d025c86a62f6e248d1883bf973</citedby><cites>FETCH-LOGICAL-c390t-a8bfdf67e90856eb4496f5f0557eb71f21dfe12d025c86a62f6e248d1883bf973</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.intimp.2017.09.030$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3541,27915,27916,45986</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29031142$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jia, Ruichun</creatorcontrib><creatorcontrib>Zhang, Haogang</creatorcontrib><creatorcontrib>Yang, Zhiping</creatorcontrib><creatorcontrib>Zhao, Hong</creatorcontrib><creatorcontrib>Liu, Fei</creatorcontrib><creatorcontrib>Wang, Hui</creatorcontrib><creatorcontrib>Miao, Meijuan</creatorcontrib><creatorcontrib>Wang, Qiushi</creatorcontrib><creatorcontrib>Liu, Yanhong</creatorcontrib><title>Protective effects of Schisandrin B on cigarette smoke-induced airway injury in mice through Nrf2 pathway</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>Schisandrin B (SchB), a dibenzocyclooctadiene derivative isolated from Schisandra chinensis, has been reported to have anti-inflammatory effects. However, the protective effects of SchB on cigarette smoke (CS)-induced lung inflammation remain unclear. This study was to investigate the effects of SchB on CS-induced lung inflammation in mice. The mice were exposed to CS to develop lung inflammation. SchB was given 1h before CS exposure daily for five consecutive days. The levels of inflammatory mediators TNF-α, IL-1β, and IL-6 in bronchoalveolar lavage fluid (BALF) were measured in this study. SOD, GSH, MPO and MDA contents were also detected. Furthermore, the expression of Nrf-2 and NF-κB were detected by western blot analysis. Histopathological analyses showed that SchB had protective effects against CS-induced lung inflammation. The levels of inflammatory mediators TNF-α, IL-1β, and IL-6 in BALF were also inhibited by SchB. CS-induced MPO activity and MDA content were inhibited by SchB. The levels of SOD and GSH were up-regulated by SchB. SchB significantly inhibited CS-induced NF-κB activation and up-regulated the expression of Nrf2 and HO-1. In conclusion, these data suggest that SchB protects against CS-induced lung inflammation by activating Nrf2 and inhibiting NF-κB signaling pathway.
•SchB had protective effects against CS-induced lung inflammation.•The levels of TNF-α and IL-1β in BALF were also inhibited by SchB.•The levels of SOD and GSH were up-regulated by SchB.•SchB significantly inhibited CS-induced NF-κB activation and up-regulated the expression of Nrf2 and HO-1.</description><subject>Alveoli</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Bronchus</subject><subject>Cells, Cultured</subject><subject>Cigarette smoke</subject><subject>Cigarette Smoking - adverse effects</subject><subject>Cigarettes</subject><subject>Cyclooctanes - therapeutic use</subject><subject>Cytokines - metabolism</subject><subject>Effects</subject><subject>GA-binding protein</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Lignans - therapeutic use</subject><subject>Lung - drug effects</subject><subject>Lung - pathology</subject><subject>Lung diseases</subject><subject>Lung inflammation</subject><subject>Lungs</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB</subject><subject>NF-κB protein</subject><subject>Nrf-2</subject><subject>Pneumonia - chemically induced</subject><subject>Pneumonia - drug therapy</subject><subject>Polycyclic Compounds - therapeutic use</subject><subject>Respiratory tract</subject><subject>Schisandra - immunology</subject><subject>Schisandrin B</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Smoke</subject><subject>Smoking</subject><subject>Tumor necrosis factor-α</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU2PFCEQhonRuOvqPzCGxIuXboFuoLmY6MavZKMm6pnQUOzQTsMI9Jr99zKZ1YMHw6Hq8FRReR-EnlLSU0LFy6UPsYb10DNCZU9UTwZyD53TSU4dlYTfbz0XsuNSqDP0qJSFNJCM9CE6Y4oMlI7sHIUvOVWwNdwABu9bV3Dy-KvdhWKiyyHiNzhFbMO1yVAr4LKmH9CF6DYLDpuQf5lbHOKy5WPBa7CA6y6n7XqHP2XP8MHUXWMeowfe7As8uasX6Pu7t98uP3RXn99_vHx91dlBkdqZafbOCwmKTFzAPI5KeO4J5xJmST2jzgNljjBuJ2EE8wLYODk6TcPslRwu0IvT3kNOPzcoVa-hWNjvTYS0FU0Vp2N7ZGzo83_QJW05tusaJaXkfBhYo8YTZXMqJYPXhxxWk281JfqoQi_6pEIfVWiidFPRxp7dLd_mFdzfoT_ZN-DVCYCWxk2ArIsNEFuqITcP2qXw_x9-A2sYnFw</recordid><startdate>201712</startdate><enddate>201712</enddate><creator>Jia, Ruichun</creator><creator>Zhang, Haogang</creator><creator>Yang, Zhiping</creator><creator>Zhao, Hong</creator><creator>Liu, Fei</creator><creator>Wang, Hui</creator><creator>Miao, Meijuan</creator><creator>Wang, Qiushi</creator><creator>Liu, Yanhong</creator><general>Elsevier B.V</general><general>Elsevier BV</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>7QO</scope><scope>7T5</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201712</creationdate><title>Protective effects of Schisandrin B on cigarette smoke-induced airway injury in mice through Nrf2 pathway</title><author>Jia, Ruichun ; Zhang, Haogang ; Yang, Zhiping ; Zhao, Hong ; Liu, Fei ; Wang, Hui ; Miao, Meijuan ; Wang, Qiushi ; Liu, Yanhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-a8bfdf67e90856eb4496f5f0557eb71f21dfe12d025c86a62f6e248d1883bf973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Alveoli</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Bronchus</topic><topic>Cells, Cultured</topic><topic>Cigarette smoke</topic><topic>Cigarette Smoking - adverse effects</topic><topic>Cigarettes</topic><topic>Cyclooctanes - therapeutic use</topic><topic>Cytokines - metabolism</topic><topic>Effects</topic><topic>GA-binding protein</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Lignans - therapeutic use</topic><topic>Lung - drug effects</topic><topic>Lung - pathology</topic><topic>Lung diseases</topic><topic>Lung inflammation</topic><topic>Lungs</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB</topic><topic>NF-κB protein</topic><topic>Nrf-2</topic><topic>Pneumonia - chemically induced</topic><topic>Pneumonia - drug therapy</topic><topic>Polycyclic Compounds - therapeutic use</topic><topic>Respiratory tract</topic><topic>Schisandra - immunology</topic><topic>Schisandrin B</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>Smoke</topic><topic>Smoking</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jia, Ruichun</creatorcontrib><creatorcontrib>Zhang, Haogang</creatorcontrib><creatorcontrib>Yang, Zhiping</creatorcontrib><creatorcontrib>Zhao, Hong</creatorcontrib><creatorcontrib>Liu, Fei</creatorcontrib><creatorcontrib>Wang, Hui</creatorcontrib><creatorcontrib>Miao, Meijuan</creatorcontrib><creatorcontrib>Wang, Qiushi</creatorcontrib><creatorcontrib>Liu, Yanhong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jia, Ruichun</au><au>Zhang, Haogang</au><au>Yang, Zhiping</au><au>Zhao, Hong</au><au>Liu, Fei</au><au>Wang, Hui</au><au>Miao, Meijuan</au><au>Wang, Qiushi</au><au>Liu, Yanhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protective effects of Schisandrin B on cigarette smoke-induced airway injury in mice through Nrf2 pathway</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2017-12</date><risdate>2017</risdate><volume>53</volume><spage>11</spage><epage>16</epage><pages>11-16</pages><issn>1567-5769</issn><eissn>1878-1705</eissn><abstract>Schisandrin B (SchB), a dibenzocyclooctadiene derivative isolated from Schisandra chinensis, has been reported to have anti-inflammatory effects. However, the protective effects of SchB on cigarette smoke (CS)-induced lung inflammation remain unclear. This study was to investigate the effects of SchB on CS-induced lung inflammation in mice. The mice were exposed to CS to develop lung inflammation. SchB was given 1h before CS exposure daily for five consecutive days. The levels of inflammatory mediators TNF-α, IL-1β, and IL-6 in bronchoalveolar lavage fluid (BALF) were measured in this study. SOD, GSH, MPO and MDA contents were also detected. Furthermore, the expression of Nrf-2 and NF-κB were detected by western blot analysis. Histopathological analyses showed that SchB had protective effects against CS-induced lung inflammation. The levels of inflammatory mediators TNF-α, IL-1β, and IL-6 in BALF were also inhibited by SchB. CS-induced MPO activity and MDA content were inhibited by SchB. The levels of SOD and GSH were up-regulated by SchB. SchB significantly inhibited CS-induced NF-κB activation and up-regulated the expression of Nrf2 and HO-1. In conclusion, these data suggest that SchB protects against CS-induced lung inflammation by activating Nrf2 and inhibiting NF-κB signaling pathway.
•SchB had protective effects against CS-induced lung inflammation.•The levels of TNF-α and IL-1β in BALF were also inhibited by SchB.•The levels of SOD and GSH were up-regulated by SchB.•SchB significantly inhibited CS-induced NF-κB activation and up-regulated the expression of Nrf2 and HO-1.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>29031142</pmid><doi>10.1016/j.intimp.2017.09.030</doi><tpages>6</tpages></addata></record> |
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| subjects | Alveoli Animals Anti-Inflammatory Agents - therapeutic use Bronchus Cells, Cultured Cigarette smoke Cigarette Smoking - adverse effects Cigarettes Cyclooctanes - therapeutic use Cytokines - metabolism Effects GA-binding protein Inflammation Interleukin 6 Lignans - therapeutic use Lung - drug effects Lung - pathology Lung diseases Lung inflammation Lungs Male Mice Mice, Inbred C57BL NF-E2-Related Factor 2 - metabolism NF-kappa B - metabolism NF-κB NF-κB protein Nrf-2 Pneumonia - chemically induced Pneumonia - drug therapy Polycyclic Compounds - therapeutic use Respiratory tract Schisandra - immunology Schisandrin B Signal Transduction Signaling Smoke Smoking Tumor necrosis factor-α |
| title | Protective effects of Schisandrin B on cigarette smoke-induced airway injury in mice through Nrf2 pathway |
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