Protective Effect of Zuojin Fang on Lung Injury Induced by Sepsis through Downregulating the JAK1/STAT3 Signaling Pathway
Lung injury was the common and serious complication of sepsis, a systemic inflammatory response syndrome caused by severe infections. Chinese medicine had unique advantages in attenuating inflammatory response, such as Zuojinfang (ZJF). ZJF was a classical compound herb formula composed of Coptidis...
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| description | Lung injury was the common and serious complication of sepsis, a systemic inflammatory response syndrome caused by severe infections. Chinese medicine had unique advantages in attenuating inflammatory response, such as Zuojinfang (ZJF). ZJF was a classical compound herb formula composed of Coptidis Rhizoma and Euodiae Fructus in a ratio of 6 : 1. In this paper, 15 ingredients in ZJF were identified and 8 of them absorbed into rat’s serum were quantified by HPLC-MS/MS. Subsequently, sepsis-induced lung injury model was replicated in rats by cecal ligation and puncture. 60 SD rats were randomly divided into 6 groups (n=10): control group (CON), sham group (Sham), model group (MOD), ZJF low-dose group (ZJF-L), ZJF high-dose group (ZJF-H), and prednisolone group (PNSL). Within the next 24 h, the levels of inflammatory factors, correlation between active ingredients and inflammatory cytokines, the pathological changes of lung tissue, and protein expression of the JAK1/STAT3 signaling pathways were analyzed one by one. Finally, the concentration order of components absorbed in rat serum was berberine > palmatine > jatrorrhizine > coptisine > evodin > chlorogenic acid > evodiamine. Compared with the MOD group, the TNF-α, IL-6, and IFN-γ in the ZJF-H group were significantly reduced (p |
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Chinese medicine had unique advantages in attenuating inflammatory response, such as Zuojinfang (ZJF). ZJF was a classical compound herb formula composed of Coptidis Rhizoma and Euodiae Fructus in a ratio of 6 : 1. In this paper, 15 ingredients in ZJF were identified and 8 of them absorbed into rat’s serum were quantified by HPLC-MS/MS. Subsequently, sepsis-induced lung injury model was replicated in rats by cecal ligation and puncture. 60 SD rats were randomly divided into 6 groups (n=10): control group (CON), sham group (Sham), model group (MOD), ZJF low-dose group (ZJF-L), ZJF high-dose group (ZJF-H), and prednisolone group (PNSL). Within the next 24 h, the levels of inflammatory factors, correlation between active ingredients and inflammatory cytokines, the pathological changes of lung tissue, and protein expression of the JAK1/STAT3 signaling pathways were analyzed one by one. Finally, the concentration order of components absorbed in rat serum was berberine > palmatine > jatrorrhizine > coptisine > evodin > chlorogenic acid > evodiamine. Compared with the MOD group, the TNF-α, IL-6, and IFN-γ in the ZJF-H group were significantly reduced (p<0.05). Moreover, the TNF-α decreased significantly accompanied by the increase of berberine, chlorogenic acid, jatrorrhizine, palmatine, evodin, and evodiamine in serum (negative correlation, p<0.05). Compared with the MOD, the area of lung injury, the expressions of JAK1, p-JAK1, STAT3, and p-STAT3 were significantly decreased under the treatment of ZJF (p<0.05). Therefore, downregulating the JAK1/STAT3 signaling pathways was a potential avenue of ZJF in reversing lung injury induced by sepsis.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2021/1419631</identifier><identifier>PMID: 33506010</identifier><language>eng</language><publisher>LONDON: Hindawi</publisher><subject>Acids ; Acute respiratory distress syndrome ; Berberine ; Biotechnology & Applied Microbiology ; Care and treatment ; Cecum ; Cellular signal transduction ; Chlorogenic acid ; Chromatography ; Complications and side effects ; Cytokines ; Drug dosages ; Drug resistance ; Herbal medicine ; High-performance liquid chromatography ; Inflammation ; Inflammatory response ; Ingredients ; Injuries ; Interleukin 6 ; Janus kinase ; Life Sciences & Biomedicine ; Liquid chromatography ; Lungs ; Medicine, Research & Experimental ; Pharmacology, Experimental ; Pharmacy ; Prednisolone ; Research & Experimental Medicine ; Respiratory agents ; Science & Technology ; Sepsis ; Signal transduction ; Signaling ; Stat3 protein ; Systemic inflammatory response syndrome ; Tumor necrosis factor-α ; γ-Interferon</subject><ispartof>BioMed research international, 2021, Vol.2021, p.1419631-12, Article 1419631</ispartof><rights>Copyright © 2021 Jiangning Yin et al.</rights><rights>COPYRIGHT 2021 John Wiley & Sons, Inc.</rights><rights>Copyright © 2021 Jiangning Yin et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2021 Jiangning Yin et al. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>4</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000611824600002</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c476t-39246323d9acabec9a43163e39013db16139c28481fb2c985dd7a1b99334d75b3</citedby><cites>FETCH-LOGICAL-c476t-39246323d9acabec9a43163e39013db16139c28481fb2c985dd7a1b99334d75b3</cites><orcidid>0000-0002-6342-165X ; 0000-0003-0258-572X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7808815/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7808815/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,4025,27928,27929,27930,39263,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33506010$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>SUN, Li-kang</contributor><contributor>Li-kang SUN</contributor><creatorcontrib>Yin, Jiangning</creatorcontrib><creatorcontrib>Yu, Zhan</creatorcontrib><creatorcontrib>Hou, Chuanyong</creatorcontrib><creatorcontrib>Peng, Yigen</creatorcontrib><creatorcontrib>Xiao, Jianpeng</creatorcontrib><creatorcontrib>Jiang, Jun</creatorcontrib><title>Protective Effect of Zuojin Fang on Lung Injury Induced by Sepsis through Downregulating the JAK1/STAT3 Signaling Pathway</title><title>BioMed research international</title><addtitle>BIOMED RES INT</addtitle><addtitle>Biomed Res Int</addtitle><description>Lung injury was the common and serious complication of sepsis, a systemic inflammatory response syndrome caused by severe infections. Chinese medicine had unique advantages in attenuating inflammatory response, such as Zuojinfang (ZJF). ZJF was a classical compound herb formula composed of Coptidis Rhizoma and Euodiae Fructus in a ratio of 6 : 1. In this paper, 15 ingredients in ZJF were identified and 8 of them absorbed into rat’s serum were quantified by HPLC-MS/MS. Subsequently, sepsis-induced lung injury model was replicated in rats by cecal ligation and puncture. 60 SD rats were randomly divided into 6 groups (n=10): control group (CON), sham group (Sham), model group (MOD), ZJF low-dose group (ZJF-L), ZJF high-dose group (ZJF-H), and prednisolone group (PNSL). Within the next 24 h, the levels of inflammatory factors, correlation between active ingredients and inflammatory cytokines, the pathological changes of lung tissue, and protein expression of the JAK1/STAT3 signaling pathways were analyzed one by one. Finally, the concentration order of components absorbed in rat serum was berberine > palmatine > jatrorrhizine > coptisine > evodin > chlorogenic acid > evodiamine. Compared with the MOD group, the TNF-α, IL-6, and IFN-γ in the ZJF-H group were significantly reduced (p<0.05). Moreover, the TNF-α decreased significantly accompanied by the increase of berberine, chlorogenic acid, jatrorrhizine, palmatine, evodin, and evodiamine in serum (negative correlation, p<0.05). Compared with the MOD, the area of lung injury, the expressions of JAK1, p-JAK1, STAT3, and p-STAT3 were significantly decreased under the treatment of ZJF (p<0.05). Therefore, downregulating the JAK1/STAT3 signaling pathways was a potential avenue of ZJF in reversing lung injury induced by sepsis.</description><subject>Acids</subject><subject>Acute respiratory distress syndrome</subject><subject>Berberine</subject><subject>Biotechnology & Applied Microbiology</subject><subject>Care and treatment</subject><subject>Cecum</subject><subject>Cellular signal transduction</subject><subject>Chlorogenic acid</subject><subject>Chromatography</subject><subject>Complications and side effects</subject><subject>Cytokines</subject><subject>Drug dosages</subject><subject>Drug resistance</subject><subject>Herbal medicine</subject><subject>High-performance liquid chromatography</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Ingredients</subject><subject>Injuries</subject><subject>Interleukin 6</subject><subject>Janus kinase</subject><subject>Life Sciences & Biomedicine</subject><subject>Liquid chromatography</subject><subject>Lungs</subject><subject>Medicine, Research & Experimental</subject><subject>Pharmacology, Experimental</subject><subject>Pharmacy</subject><subject>Prednisolone</subject><subject>Research & Experimental Medicine</subject><subject>Respiratory agents</subject><subject>Science & Technology</subject><subject>Sepsis</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Stat3 protein</subject><subject>Systemic inflammatory response syndrome</subject><subject>Tumor necrosis 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Effect of Zuojin Fang on Lung Injury Induced by Sepsis through Downregulating the JAK1/STAT3 Signaling Pathway</title><author>Yin, Jiangning ; Yu, Zhan ; Hou, Chuanyong ; Peng, Yigen ; Xiao, Jianpeng ; Jiang, Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-39246323d9acabec9a43163e39013db16139c28481fb2c985dd7a1b99334d75b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acids</topic><topic>Acute respiratory distress syndrome</topic><topic>Berberine</topic><topic>Biotechnology & Applied Microbiology</topic><topic>Care and treatment</topic><topic>Cecum</topic><topic>Cellular signal transduction</topic><topic>Chlorogenic acid</topic><topic>Chromatography</topic><topic>Complications and side effects</topic><topic>Cytokines</topic><topic>Drug dosages</topic><topic>Drug resistance</topic><topic>Herbal medicine</topic><topic>High-performance liquid chromatography</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Ingredients</topic><topic>Injuries</topic><topic>Interleukin 6</topic><topic>Janus kinase</topic><topic>Life Sciences & Biomedicine</topic><topic>Liquid chromatography</topic><topic>Lungs</topic><topic>Medicine, Research & Experimental</topic><topic>Pharmacology, Experimental</topic><topic>Pharmacy</topic><topic>Prednisolone</topic><topic>Research & Experimental Medicine</topic><topic>Respiratory agents</topic><topic>Science & Technology</topic><topic>Sepsis</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Stat3 protein</topic><topic>Systemic inflammatory response syndrome</topic><topic>Tumor necrosis factor-α</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yin, Jiangning</creatorcontrib><creatorcontrib>Yu, Zhan</creatorcontrib><creatorcontrib>Hou, Chuanyong</creatorcontrib><creatorcontrib>Peng, 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Sepsis through Downregulating the JAK1/STAT3 Signaling Pathway</atitle><jtitle>BioMed research international</jtitle><stitle>BIOMED RES INT</stitle><addtitle>Biomed Res Int</addtitle><date>2021</date><risdate>2021</risdate><volume>2021</volume><spage>1419631</spage><epage>12</epage><pages>1419631-12</pages><artnum>1419631</artnum><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Lung injury was the common and serious complication of sepsis, a systemic inflammatory response syndrome caused by severe infections. Chinese medicine had unique advantages in attenuating inflammatory response, such as Zuojinfang (ZJF). ZJF was a classical compound herb formula composed of Coptidis Rhizoma and Euodiae Fructus in a ratio of 6 : 1. In this paper, 15 ingredients in ZJF were identified and 8 of them absorbed into rat’s serum were quantified by HPLC-MS/MS. Subsequently, sepsis-induced lung injury model was replicated in rats by cecal ligation and puncture. 60 SD rats were randomly divided into 6 groups (n=10): control group (CON), sham group (Sham), model group (MOD), ZJF low-dose group (ZJF-L), ZJF high-dose group (ZJF-H), and prednisolone group (PNSL). Within the next 24 h, the levels of inflammatory factors, correlation between active ingredients and inflammatory cytokines, the pathological changes of lung tissue, and protein expression of the JAK1/STAT3 signaling pathways were analyzed one by one. Finally, the concentration order of components absorbed in rat serum was berberine > palmatine > jatrorrhizine > coptisine > evodin > chlorogenic acid > evodiamine. Compared with the MOD group, the TNF-α, IL-6, and IFN-γ in the ZJF-H group were significantly reduced (p<0.05). Moreover, the TNF-α decreased significantly accompanied by the increase of berberine, chlorogenic acid, jatrorrhizine, palmatine, evodin, and evodiamine in serum (negative correlation, p<0.05). Compared with the MOD, the area of lung injury, the expressions of JAK1, p-JAK1, STAT3, and p-STAT3 were significantly decreased under the treatment of ZJF (p<0.05). Therefore, downregulating the JAK1/STAT3 signaling pathways was a potential avenue of ZJF in reversing lung injury induced by sepsis.</abstract><cop>LONDON</cop><pub>Hindawi</pub><pmid>33506010</pmid><doi>10.1155/2021/1419631</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-6342-165X</orcidid><orcidid>https://orcid.org/0000-0003-0258-572X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Acids Acute respiratory distress syndrome Berberine Biotechnology & Applied Microbiology Care and treatment Cecum Cellular signal transduction Chlorogenic acid Chromatography Complications and side effects Cytokines Drug dosages Drug resistance Herbal medicine High-performance liquid chromatography Inflammation Inflammatory response Ingredients Injuries Interleukin 6 Janus kinase Life Sciences & Biomedicine Liquid chromatography Lungs Medicine, Research & Experimental Pharmacology, Experimental Pharmacy Prednisolone Research & Experimental Medicine Respiratory agents Science & Technology Sepsis Signal transduction Signaling Stat3 protein Systemic inflammatory response syndrome Tumor necrosis factor-α γ-Interferon |
| title | Protective Effect of Zuojin Fang on Lung Injury Induced by Sepsis through Downregulating the JAK1/STAT3 Signaling Pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-12T09%3A14%3A36IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_webof&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Protective%20Effect%20of%20Zuojin%20Fang%20on%20Lung%20Injury%20Induced%20by%20Sepsis%20through%20Downregulating%20the%20JAK1/STAT3%20Signaling%20Pathway&rft.jtitle=BioMed%20research%20international&rft.au=Yin,%20Jiangning&rft.date=2021&rft.volume=2021&rft.spage=1419631&rft.epage=12&rft.pages=1419631-12&rft.artnum=1419631&rft.issn=2314-6133&rft.eissn=2314-6141&rft_id=info:doi/10.1155/2021/1419631&rft_dat=%3Cgale_webof%3EA696727773%3C/gale_webof%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2478358054&rft_id=info:pmid/33506010&rft_galeid=A696727773&rfr_iscdi=true |