Role of Nrf2/ARE pathway in protective effect of electroacupuncture against endotoxic shock-induced acute lung injury in rabbits
NF-E2 related factor 2 (Nrf2) is a major transcription factor and acts as a key regulator of antioxidant genes to exogenous stimulations. The aim of current study was to determine whether Nrf2/ARE pathway is involved in the protective effect of electroacupuncture on the injured lung in a rabbit mode...
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| creator | Yu, Jian-bo Shi, Jia Gong, Li-rong Dong, Shu-an Xu, Yan Zhang, Yuan Cao, Xin-shun Wu, Li-li |
| description | NF-E2 related factor 2 (Nrf2) is a major transcription factor and acts as a key regulator of antioxidant genes to exogenous stimulations. The aim of current study was to determine whether Nrf2/ARE pathway is involved in the protective effect of electroacupuncture on the injured lung in a rabbit model of endotoxic shock. A dose of lipopolysaccharide (LPS) 5 mg/kg was administered intravenously to replicate the model of acute lung injury induced by endotoxic shock. Electroacupuncture pretreatment was handled bilaterally at Zusanli and Feishu acupoints for five consecutive days while sham electroacupuncture punctured at non-acupoints. Fourty anesthetized New England male rabbits were randomized into normal control group (group C), LPS group (group L), electroacupuncture + LPS group (group EL) and sham electroacupuncture + LPS (group SEL). At 6 h after LPS administration, the animals were sacrificed and the blood samples were collected for biochemical measurements. The lungs were removed for calculation of wet-to-dry weight ratios (W/D), histopathologic examination, determination of heme oxygenase (HO)-1 protein and mRNA, Nrf2 total and nucleoprotein, as well as Nrf2 mRNA expression, and evaluation of the intracellular distribution of Nrf2 nucleoprotein. LPS caused extensive morphologic lung damage, which was lessened by electroacupuncture treatment. Besides, lung W/D ratios were significantly decreased, the level of malondialdehyde was inhibited, plasma levels of TNF-α and interleukin-6 were decreased, while the activities of superoxide dismutase, glutathione peroxidase and catalase were enhanced in the electroacupucnture treated animals. In addition, electroacupuncture stimulation distinctly increased the expressions of HO-1 and Nrf2 protein including Nrf2 total protein and nucleoprotein as well as mRNA in lung tissue, while these effects were blunted in the sham electroacupuncture group. We concluded that electroacupuncture treatment at ST36 and BL13 effectively attenuates lung injury in a rabbit model of endotoxic shock through activation of Nrf2/ARE pathway and following up-regulation of HO-1 expression. |
| doi_str_mv | 10.1371/journal.pone.0104924 |
| format | Article |
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The aim of current study was to determine whether Nrf2/ARE pathway is involved in the protective effect of electroacupuncture on the injured lung in a rabbit model of endotoxic shock. A dose of lipopolysaccharide (LPS) 5 mg/kg was administered intravenously to replicate the model of acute lung injury induced by endotoxic shock. Electroacupuncture pretreatment was handled bilaterally at Zusanli and Feishu acupoints for five consecutive days while sham electroacupuncture punctured at non-acupoints. Fourty anesthetized New England male rabbits were randomized into normal control group (group C), LPS group (group L), electroacupuncture + LPS group (group EL) and sham electroacupuncture + LPS (group SEL). At 6 h after LPS administration, the animals were sacrificed and the blood samples were collected for biochemical measurements. The lungs were removed for calculation of wet-to-dry weight ratios (W/D), histopathologic examination, determination of heme oxygenase (HO)-1 protein and mRNA, Nrf2 total and nucleoprotein, as well as Nrf2 mRNA expression, and evaluation of the intracellular distribution of Nrf2 nucleoprotein. LPS caused extensive morphologic lung damage, which was lessened by electroacupuncture treatment. Besides, lung W/D ratios were significantly decreased, the level of malondialdehyde was inhibited, plasma levels of TNF-α and interleukin-6 were decreased, while the activities of superoxide dismutase, glutathione peroxidase and catalase were enhanced in the electroacupucnture treated animals. In addition, electroacupuncture stimulation distinctly increased the expressions of HO-1 and Nrf2 protein including Nrf2 total protein and nucleoprotein as well as mRNA in lung tissue, while these effects were blunted in the sham electroacupuncture group. We concluded that electroacupuncture treatment at ST36 and BL13 effectively attenuates lung injury in a rabbit model of endotoxic shock through activation of Nrf2/ARE pathway and following up-regulation of HO-1 expression.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0104924</identifier><identifier>PMID: 25115759</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acupuncture ; Acute Lung Injury - etiology ; Acute Lung Injury - physiopathology ; Acute Lung Injury - prevention & control ; Adult respiratory distress syndrome ; Analysis ; Anesthesiology ; Animals ; Antioxidant Response Elements ; Antioxidants ; Antioxidants (Nutrients) ; Biology and Life Sciences ; Carbon monoxide ; Catalase ; Catheters ; Disease Models, Animal ; Edema ; Electroacupuncture ; Endotoxemia ; Enzymes ; Gene expression ; Glutathione ; Glutathione peroxidase ; Heme ; Heme Oxygenase-1 - metabolism ; Hospitals ; Injuries ; Interleukin 6 ; Interleukin-6 - blood ; Laboratory animals ; Lipopolysaccharides ; Lung - pathology ; Lung - physiopathology ; Lungs ; Male ; Malondialdehyde ; Malondialdehyde - metabolism ; Medicine and Health Sciences ; Mortality ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; NRF2 protein ; Oxidative stress ; Oxygenase ; Peroxidase ; Plasma levels ; Rabbits ; Respiratory distress syndrome ; RNA ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Rodents ; Science Policy ; Sepsis ; Septic shock ; Shock ; Shock, Septic - complications ; Shock, Septic - physiopathology ; Shock, Septic - therapy ; Signal Transduction ; Superoxide dismutase ; Superoxide Dismutase - metabolism ; Superoxides ; Tumor Necrosis Factor-alpha - blood ; Tumor necrosis factor-α</subject><ispartof>PloS one, 2014-08, Vol.9 (8), p.e104924-e104924</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Yu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Yu et al 2014 Yu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-2854741dcf7a8388f706009e9d3356a3727503873de8f6b767a49f25826c92d83</citedby><cites>FETCH-LOGICAL-c692t-2854741dcf7a8388f706009e9d3356a3727503873de8f6b767a49f25826c92d83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4130631/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4130631/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25115759$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu, Jian-bo</creatorcontrib><creatorcontrib>Shi, Jia</creatorcontrib><creatorcontrib>Gong, Li-rong</creatorcontrib><creatorcontrib>Dong, Shu-an</creatorcontrib><creatorcontrib>Xu, Yan</creatorcontrib><creatorcontrib>Zhang, Yuan</creatorcontrib><creatorcontrib>Cao, Xin-shun</creatorcontrib><creatorcontrib>Wu, Li-li</creatorcontrib><title>Role of Nrf2/ARE pathway in protective effect of electroacupuncture against endotoxic shock-induced acute lung injury in rabbits</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>NF-E2 related factor 2 (Nrf2) is a major transcription factor and acts as a key regulator of antioxidant genes to exogenous stimulations. The aim of current study was to determine whether Nrf2/ARE pathway is involved in the protective effect of electroacupuncture on the injured lung in a rabbit model of endotoxic shock. A dose of lipopolysaccharide (LPS) 5 mg/kg was administered intravenously to replicate the model of acute lung injury induced by endotoxic shock. Electroacupuncture pretreatment was handled bilaterally at Zusanli and Feishu acupoints for five consecutive days while sham electroacupuncture punctured at non-acupoints. Fourty anesthetized New England male rabbits were randomized into normal control group (group C), LPS group (group L), electroacupuncture + LPS group (group EL) and sham electroacupuncture + LPS (group SEL). At 6 h after LPS administration, the animals were sacrificed and the blood samples were collected for biochemical measurements. The lungs were removed for calculation of wet-to-dry weight ratios (W/D), histopathologic examination, determination of heme oxygenase (HO)-1 protein and mRNA, Nrf2 total and nucleoprotein, as well as Nrf2 mRNA expression, and evaluation of the intracellular distribution of Nrf2 nucleoprotein. LPS caused extensive morphologic lung damage, which was lessened by electroacupuncture treatment. Besides, lung W/D ratios were significantly decreased, the level of malondialdehyde was inhibited, plasma levels of TNF-α and interleukin-6 were decreased, while the activities of superoxide dismutase, glutathione peroxidase and catalase were enhanced in the electroacupucnture treated animals. In addition, electroacupuncture stimulation distinctly increased the expressions of HO-1 and Nrf2 protein including Nrf2 total protein and nucleoprotein as well as mRNA in lung tissue, while these effects were blunted in the sham electroacupuncture group. We concluded that electroacupuncture treatment at ST36 and BL13 effectively attenuates lung injury in a rabbit model of endotoxic shock through activation of Nrf2/ARE pathway and following up-regulation of HO-1 expression.</description><subject>Acupuncture</subject><subject>Acute Lung Injury - etiology</subject><subject>Acute Lung Injury - physiopathology</subject><subject>Acute Lung Injury - prevention & control</subject><subject>Adult respiratory distress syndrome</subject><subject>Analysis</subject><subject>Anesthesiology</subject><subject>Animals</subject><subject>Antioxidant Response Elements</subject><subject>Antioxidants</subject><subject>Antioxidants (Nutrients)</subject><subject>Biology and Life Sciences</subject><subject>Carbon monoxide</subject><subject>Catalase</subject><subject>Catheters</subject><subject>Disease Models, Animal</subject><subject>Edema</subject><subject>Electroacupuncture</subject><subject>Endotoxemia</subject><subject>Enzymes</subject><subject>Gene expression</subject><subject>Glutathione</subject><subject>Glutathione peroxidase</subject><subject>Heme</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Hospitals</subject><subject>Injuries</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - blood</subject><subject>Laboratory animals</subject><subject>Lipopolysaccharides</subject><subject>Lung - pathology</subject><subject>Lung - physiopathology</subject><subject>Lungs</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Malondialdehyde - metabolism</subject><subject>Medicine and Health Sciences</subject><subject>Mortality</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>NRF2 protein</subject><subject>Oxidative stress</subject><subject>Oxygenase</subject><subject>Peroxidase</subject><subject>Plasma levels</subject><subject>Rabbits</subject><subject>Respiratory distress syndrome</subject><subject>RNA</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Science Policy</subject><subject>Sepsis</subject><subject>Septic shock</subject><subject>Shock</subject><subject>Shock, Septic - complications</subject><subject>Shock, Septic - physiopathology</subject><subject>Shock, Septic - therapy</subject><subject>Signal Transduction</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Superoxides</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor necrosis factor-α</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk99vUyEUx2-Mxs3qf2D0JiZGH9rx6wL3xaRZpi5ZXDJ_vBLKPbTUW6jAndubf7p065bW7MFAwgE-53vgwKmqlxhNMBX4aBmG6HU_WQcPE4QRawl7VB3ilpIxJ4g-3rEPqmcpLRFqqOT8aXVAGowb0bSH1Z-L0EMdbP0lWnI0vTip1zovfuvr2vl6HUMGk90l1GBtsTYg9MWIQZthPXiThwi1nmvnU67BdyGHK2fqtAjm59j5bjDQ1YXNUPeDnxfV5RBvxKOezVxOz6snVvcJXmzHUfX948m348_js_NPp8fTs7HhLcljIhsmGO6MFVpSKa1AHKEW2o7ShmsqiGgQlYJ2IC2fCS40ay1pJOGmJZ2ko-r1re66D0ltk5cUQZhKgmnpo-r0luiCXqp1dCsdr1XQTt0shDhXOmZnelBECAbANRMzzZpWambKhFgktUElU0XrwzbaMFtBZ8DnqPs90f0d7xZqHi4VwxRxujnMu61ADL8GSFmtXDLQ99pDGJLCTUMFkoTwgr75B334dltqrssFnLehxDUbUTVlWHLKWkEKNXmAKq2DlTPlp1lX1vcc3u85FCbDVZ7rISV1-vXi_9nzH_vs2x12AbrPixT6Ibvg0z7IbkETQ0oR7H2SMVKbQrnLhtoUitoWSnF7tftA9053lUH_AnOVDdg</recordid><startdate>20140812</startdate><enddate>20140812</enddate><creator>Yu, Jian-bo</creator><creator>Shi, Jia</creator><creator>Gong, Li-rong</creator><creator>Dong, Shu-an</creator><creator>Xu, Yan</creator><creator>Zhang, Yuan</creator><creator>Cao, Xin-shun</creator><creator>Wu, Li-li</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</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>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140812</creationdate><title>Role of Nrf2/ARE pathway in protective effect of electroacupuncture against endotoxic shock-induced acute lung injury in rabbits</title><author>Yu, Jian-bo ; Shi, Jia ; Gong, Li-rong ; Dong, Shu-an ; Xu, Yan ; Zhang, Yuan ; Cao, Xin-shun ; Wu, Li-li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-2854741dcf7a8388f706009e9d3356a3727503873de8f6b767a49f25826c92d83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Acupuncture</topic><topic>Acute Lung Injury - etiology</topic><topic>Acute Lung Injury - physiopathology</topic><topic>Acute Lung Injury - prevention & control</topic><topic>Adult respiratory distress syndrome</topic><topic>Analysis</topic><topic>Anesthesiology</topic><topic>Animals</topic><topic>Antioxidant Response Elements</topic><topic>Antioxidants</topic><topic>Antioxidants (Nutrients)</topic><topic>Biology and Life Sciences</topic><topic>Carbon monoxide</topic><topic>Catalase</topic><topic>Catheters</topic><topic>Disease Models, Animal</topic><topic>Edema</topic><topic>Electroacupuncture</topic><topic>Endotoxemia</topic><topic>Enzymes</topic><topic>Gene expression</topic><topic>Glutathione</topic><topic>Glutathione peroxidase</topic><topic>Heme</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Hospitals</topic><topic>Injuries</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - blood</topic><topic>Laboratory animals</topic><topic>Lipopolysaccharides</topic><topic>Lung - pathology</topic><topic>Lung - physiopathology</topic><topic>Lungs</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Malondialdehyde - metabolism</topic><topic>Medicine and Health Sciences</topic><topic>Mortality</topic><topic>NF-E2-Related Factor 2 - genetics</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>NRF2 protein</topic><topic>Oxidative stress</topic><topic>Oxygenase</topic><topic>Peroxidase</topic><topic>Plasma levels</topic><topic>Rabbits</topic><topic>Respiratory distress syndrome</topic><topic>RNA</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Science Policy</topic><topic>Sepsis</topic><topic>Septic shock</topic><topic>Shock</topic><topic>Shock, Septic - complications</topic><topic>Shock, Septic - physiopathology</topic><topic>Shock, Septic - therapy</topic><topic>Signal Transduction</topic><topic>Superoxide dismutase</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Superoxides</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Jian-bo</creatorcontrib><creatorcontrib>Shi, Jia</creatorcontrib><creatorcontrib>Gong, Li-rong</creatorcontrib><creatorcontrib>Dong, Shu-an</creatorcontrib><creatorcontrib>Xu, Yan</creatorcontrib><creatorcontrib>Zhang, Yuan</creatorcontrib><creatorcontrib>Cao, Xin-shun</creatorcontrib><creatorcontrib>Wu, Li-li</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</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>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Jian-bo</au><au>Shi, Jia</au><au>Gong, Li-rong</au><au>Dong, Shu-an</au><au>Xu, Yan</au><au>Zhang, Yuan</au><au>Cao, Xin-shun</au><au>Wu, Li-li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of Nrf2/ARE pathway in protective effect of electroacupuncture against endotoxic shock-induced acute lung injury in rabbits</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-08-12</date><risdate>2014</risdate><volume>9</volume><issue>8</issue><spage>e104924</spage><epage>e104924</epage><pages>e104924-e104924</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>NF-E2 related factor 2 (Nrf2) is a major transcription factor and acts as a key regulator of antioxidant genes to exogenous stimulations. The aim of current study was to determine whether Nrf2/ARE pathway is involved in the protective effect of electroacupuncture on the injured lung in a rabbit model of endotoxic shock. A dose of lipopolysaccharide (LPS) 5 mg/kg was administered intravenously to replicate the model of acute lung injury induced by endotoxic shock. Electroacupuncture pretreatment was handled bilaterally at Zusanli and Feishu acupoints for five consecutive days while sham electroacupuncture punctured at non-acupoints. Fourty anesthetized New England male rabbits were randomized into normal control group (group C), LPS group (group L), electroacupuncture + LPS group (group EL) and sham electroacupuncture + LPS (group SEL). At 6 h after LPS administration, the animals were sacrificed and the blood samples were collected for biochemical measurements. The lungs were removed for calculation of wet-to-dry weight ratios (W/D), histopathologic examination, determination of heme oxygenase (HO)-1 protein and mRNA, Nrf2 total and nucleoprotein, as well as Nrf2 mRNA expression, and evaluation of the intracellular distribution of Nrf2 nucleoprotein. LPS caused extensive morphologic lung damage, which was lessened by electroacupuncture treatment. Besides, lung W/D ratios were significantly decreased, the level of malondialdehyde was inhibited, plasma levels of TNF-α and interleukin-6 were decreased, while the activities of superoxide dismutase, glutathione peroxidase and catalase were enhanced in the electroacupucnture treated animals. In addition, electroacupuncture stimulation distinctly increased the expressions of HO-1 and Nrf2 protein including Nrf2 total protein and nucleoprotein as well as mRNA in lung tissue, while these effects were blunted in the sham electroacupuncture group. We concluded that electroacupuncture treatment at ST36 and BL13 effectively attenuates lung injury in a rabbit model of endotoxic shock through activation of Nrf2/ARE pathway and following up-regulation of HO-1 expression.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25115759</pmid><doi>10.1371/journal.pone.0104924</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-08, Vol.9 (8), p.e104924-e104924 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2013821321 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Acupuncture Acute Lung Injury - etiology Acute Lung Injury - physiopathology Acute Lung Injury - prevention & control Adult respiratory distress syndrome Analysis Anesthesiology Animals Antioxidant Response Elements Antioxidants Antioxidants (Nutrients) Biology and Life Sciences Carbon monoxide Catalase Catheters Disease Models, Animal Edema Electroacupuncture Endotoxemia Enzymes Gene expression Glutathione Glutathione peroxidase Heme Heme Oxygenase-1 - metabolism Hospitals Injuries Interleukin 6 Interleukin-6 - blood Laboratory animals Lipopolysaccharides Lung - pathology Lung - physiopathology Lungs Male Malondialdehyde Malondialdehyde - metabolism Medicine and Health Sciences Mortality NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism NRF2 protein Oxidative stress Oxygenase Peroxidase Plasma levels Rabbits Respiratory distress syndrome RNA RNA, Messenger - genetics RNA, Messenger - metabolism Rodents Science Policy Sepsis Septic shock Shock Shock, Septic - complications Shock, Septic - physiopathology Shock, Septic - therapy Signal Transduction Superoxide dismutase Superoxide Dismutase - metabolism Superoxides Tumor Necrosis Factor-alpha - blood Tumor necrosis factor-α |
| title | Role of Nrf2/ARE pathway in protective effect of electroacupuncture against endotoxic shock-induced acute lung injury in rabbits |
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