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Polygalaxanthone III downregulates inflammation in the lipopolysaccharide-stimulated RAW264.7 macrophages: A quantibody array analysis
Polygala japonica Houtt. (PJ), a member of the Polygala L. family that is suggested to exhibit detoxification properties in traditional Chinese medicine, is often used to treat upper respiratory tract infections. The anti-inflammatory effects of four main components of PJ (POL, PS-XLIX, PS-E, and PS...
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| Published in: | Journal of pharmacological sciences 2021-10, Vol.147 (2), p.184-191 |
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| cites | cdi_FETCH-LOGICAL-c490t-e71cab3f3e77a2d0d4175f95046e417ff43455af8d9ac8361c79c1e3b4d6e8c93 |
| container_end_page | 191 |
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| creator | Wu, Yinan Fu, Hongwei Yang, Xiaobin Leng, Fang Huang, Yadong Deng, Hong Xiang, Qi Zhang, Shu |
| description | Polygala japonica Houtt. (PJ), a member of the Polygala L. family that is suggested to exhibit detoxification properties in traditional Chinese medicine, is often used to treat upper respiratory tract infections. The anti-inflammatory effects of four main components of PJ (POL, PS-XLIX, PS-E, and PS-F) were examined using the LPS(0.3 μg·mL−1)-stimulated RAW264.7 macrophage model. The levels of NO, ROS, and iNOS were examined to analyze the anti-inflammatory activity of POL. Additionally, the levels of extracellular inflammation-related cytokines and chemokines were measured using quantibody array. The KEGG pathway analysis was performed to examine the anti-inflammatory mechanism of POL. The levels of NO in the POL-pretreated group were significantly downregulated when compared with those in the PS-E-pretreated, PS-F-pretreated, and PS-XLIX-pretreated groups. POL significantly inhibited the changes of iNOS, ROS, and inflammatory factors caused by LPS stimulation (p |
| doi_str_mv | 10.1016/j.jphs.2021.06.010 |
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(PJ), a member of the Polygala L. family that is suggested to exhibit detoxification properties in traditional Chinese medicine, is often used to treat upper respiratory tract infections. The anti-inflammatory effects of four main components of PJ (POL, PS-XLIX, PS-E, and PS-F) were examined using the LPS(0.3 μg·mL−1)-stimulated RAW264.7 macrophage model. The levels of NO, ROS, and iNOS were examined to analyze the anti-inflammatory activity of POL. Additionally, the levels of extracellular inflammation-related cytokines and chemokines were measured using quantibody array. The KEGG pathway analysis was performed to examine the anti-inflammatory mechanism of POL. The levels of NO in the POL-pretreated group were significantly downregulated when compared with those in the PS-E-pretreated, PS-F-pretreated, and PS-XLIX-pretreated groups. POL significantly inhibited the changes of iNOS, ROS, and inflammatory factors caused by LPS stimulation (p < 0.001). The expression levels of IL21 and GM-CSF were examined using qPCR, while those of JAK-STAT signaling pathway-related proteins in the LPS-stimulated RAW264.7 macrophages were analyzed using western blotting. POL significantly downregulated the expression of IL-21 and GM-CSF. The anti-inflammatory mechanism of POL is mediated through the JAK-STAT pathway. Thus, this study demonstrated that POL is an anti-inflammatory component of PJ and elucidated its mechanism.</description><identifier>ISSN: 1347-8613</identifier><identifier>EISSN: 1347-8648</identifier><identifier>DOI: 10.1016/j.jphs.2021.06.010</identifier><identifier>PMID: 34384566</identifier><language>eng</language><publisher>Japan: Elsevier B.V</publisher><subject>Animals ; Anti-Inflammatory Agents ; Cytokines - genetics ; Cytokines - metabolism ; Down-Regulation - drug effects ; Drugs, Chinese Herbal - pharmacology ; Gene Expression - drug effects ; Glycosides - pharmacology ; IL21 ; Inflammation - etiology ; Inflammation - genetics ; Inflammation Mediators - metabolism ; Inflammation modulation ; Interleukins - genetics ; Interleukins - metabolism ; Lipopolysaccharides - adverse effects ; Mice ; Nitric Oxide - genetics ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type II - genetics ; Nitric Oxide Synthase Type II - metabolism ; Polygala - chemistry ; Polygala japonica Houtt ; Polygalaxanthone III ; Quantibody array ; RAW 264.7 Cells ; Reactive Oxygen Species - metabolism ; Signal Transduction - drug effects ; Xanthones - pharmacology</subject><ispartof>Journal of pharmacological sciences, 2021-10, Vol.147 (2), p.184-191</ispartof><rights>2021 The Authors</rights><rights>Copyright © 2021 The Authors. Production and hosting by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-e71cab3f3e77a2d0d4175f95046e417ff43455af8d9ac8361c79c1e3b4d6e8c93</citedby><cites>FETCH-LOGICAL-c490t-e71cab3f3e77a2d0d4175f95046e417ff43455af8d9ac8361c79c1e3b4d6e8c93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1347861321000669$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3536,27901,27902,45756</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34384566$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Yinan</creatorcontrib><creatorcontrib>Fu, Hongwei</creatorcontrib><creatorcontrib>Yang, Xiaobin</creatorcontrib><creatorcontrib>Leng, Fang</creatorcontrib><creatorcontrib>Huang, Yadong</creatorcontrib><creatorcontrib>Deng, Hong</creatorcontrib><creatorcontrib>Xiang, Qi</creatorcontrib><creatorcontrib>Zhang, Shu</creatorcontrib><title>Polygalaxanthone III downregulates inflammation in the lipopolysaccharide-stimulated RAW264.7 macrophages: A quantibody array analysis</title><title>Journal of pharmacological sciences</title><addtitle>J Pharmacol Sci</addtitle><description>Polygala japonica Houtt. (PJ), a member of the Polygala L. family that is suggested to exhibit detoxification properties in traditional Chinese medicine, is often used to treat upper respiratory tract infections. The anti-inflammatory effects of four main components of PJ (POL, PS-XLIX, PS-E, and PS-F) were examined using the LPS(0.3 μg·mL−1)-stimulated RAW264.7 macrophage model. The levels of NO, ROS, and iNOS were examined to analyze the anti-inflammatory activity of POL. Additionally, the levels of extracellular inflammation-related cytokines and chemokines were measured using quantibody array. The KEGG pathway analysis was performed to examine the anti-inflammatory mechanism of POL. The levels of NO in the POL-pretreated group were significantly downregulated when compared with those in the PS-E-pretreated, PS-F-pretreated, and PS-XLIX-pretreated groups. POL significantly inhibited the changes of iNOS, ROS, and inflammatory factors caused by LPS stimulation (p < 0.001). The expression levels of IL21 and GM-CSF were examined using qPCR, while those of JAK-STAT signaling pathway-related proteins in the LPS-stimulated RAW264.7 macrophages were analyzed using western blotting. POL significantly downregulated the expression of IL-21 and GM-CSF. The anti-inflammatory mechanism of POL is mediated through the JAK-STAT pathway. Thus, this study demonstrated that POL is an anti-inflammatory component of PJ and elucidated its mechanism.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Down-Regulation - drug effects</subject><subject>Drugs, Chinese Herbal - pharmacology</subject><subject>Gene Expression - drug effects</subject><subject>Glycosides - pharmacology</subject><subject>IL21</subject><subject>Inflammation - etiology</subject><subject>Inflammation - genetics</subject><subject>Inflammation Mediators - metabolism</subject><subject>Inflammation modulation</subject><subject>Interleukins - genetics</subject><subject>Interleukins - metabolism</subject><subject>Lipopolysaccharides - adverse effects</subject><subject>Mice</subject><subject>Nitric Oxide - genetics</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Polygala - chemistry</subject><subject>Polygala japonica Houtt</subject><subject>Polygalaxanthone III</subject><subject>Quantibody array</subject><subject>RAW 264.7 Cells</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Xanthones - pharmacology</subject><issn>1347-8613</issn><issn>1347-8648</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNp9kcFu1DAQhiMEoqXwAhxQjlwS7NhxEsRlVVGIVAmEQBytiT3eOEri1E6AfQGeu95u2SMXe8b6_2_k-ZPkNSU5JVS8G_Jh6UNekILmROSEkifJJWW8ymrB66fnmrKL5EUIAyFFHX3PkwvGWc1LIS6Tv1_deNjDCH9gXns3Y9q2bard79njfhthxZDa2YwwTbBaN8cmXXtMR7u4JVoDKNWDtxqzsNrpwaHTb7ufheB5lU6gvFt62GN4n-7Suy1OsZ3ThxS8h3jOEBk2vEyeGRgDvnq8r5IfNx-_X3_Obr98aq93t5niDVkzrKiCjhmGVQWFJprTqjRNSbjAWBrDGS9LMLVuQNVMUFU1iiLruBZYq4ZdJe2Jqx0McvF2An-QDqx8eHB-L8GvVo0oqy7O6JCLkpVcaNaAoEabyCZKmU5F1tsTa_HubsOwyskGheMIM7otyKIUlNc1K0WUFidp3EYIHs15NCXymKUc5DFLecxSEiFjltH05pG_dRPqs-VfeFHw4STAuLFfFr0MyuKsUFuPao1fsv_j3wMSrrMI</recordid><startdate>202110</startdate><enddate>202110</enddate><creator>Wu, Yinan</creator><creator>Fu, Hongwei</creator><creator>Yang, Xiaobin</creator><creator>Leng, Fang</creator><creator>Huang, Yadong</creator><creator>Deng, Hong</creator><creator>Xiang, Qi</creator><creator>Zhang, Shu</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope><scope>DOA</scope></search><sort><creationdate>202110</creationdate><title>Polygalaxanthone III downregulates inflammation in the lipopolysaccharide-stimulated RAW264.7 macrophages: A quantibody array analysis</title><author>Wu, Yinan ; Fu, Hongwei ; Yang, Xiaobin ; Leng, Fang ; Huang, Yadong ; Deng, Hong ; Xiang, Qi ; Zhang, Shu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c490t-e71cab3f3e77a2d0d4175f95046e417ff43455af8d9ac8361c79c1e3b4d6e8c93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Down-Regulation - drug effects</topic><topic>Drugs, Chinese Herbal - pharmacology</topic><topic>Gene Expression - drug effects</topic><topic>Glycosides - pharmacology</topic><topic>IL21</topic><topic>Inflammation - etiology</topic><topic>Inflammation - genetics</topic><topic>Inflammation Mediators - metabolism</topic><topic>Inflammation modulation</topic><topic>Interleukins - genetics</topic><topic>Interleukins - metabolism</topic><topic>Lipopolysaccharides - adverse effects</topic><topic>Mice</topic><topic>Nitric Oxide - genetics</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Polygala - chemistry</topic><topic>Polygala japonica Houtt</topic><topic>Polygalaxanthone III</topic><topic>Quantibody array</topic><topic>RAW 264.7 Cells</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Xanthones - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Yinan</creatorcontrib><creatorcontrib>Fu, Hongwei</creatorcontrib><creatorcontrib>Yang, Xiaobin</creatorcontrib><creatorcontrib>Leng, Fang</creatorcontrib><creatorcontrib>Huang, Yadong</creatorcontrib><creatorcontrib>Deng, Hong</creatorcontrib><creatorcontrib>Xiang, Qi</creatorcontrib><creatorcontrib>Zhang, Shu</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Journal of pharmacological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Yinan</au><au>Fu, Hongwei</au><au>Yang, Xiaobin</au><au>Leng, Fang</au><au>Huang, Yadong</au><au>Deng, Hong</au><au>Xiang, Qi</au><au>Zhang, Shu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Polygalaxanthone III downregulates inflammation in the lipopolysaccharide-stimulated RAW264.7 macrophages: A quantibody array analysis</atitle><jtitle>Journal of pharmacological sciences</jtitle><addtitle>J Pharmacol Sci</addtitle><date>2021-10</date><risdate>2021</risdate><volume>147</volume><issue>2</issue><spage>184</spage><epage>191</epage><pages>184-191</pages><issn>1347-8613</issn><eissn>1347-8648</eissn><abstract>Polygala japonica Houtt. (PJ), a member of the Polygala L. family that is suggested to exhibit detoxification properties in traditional Chinese medicine, is often used to treat upper respiratory tract infections. The anti-inflammatory effects of four main components of PJ (POL, PS-XLIX, PS-E, and PS-F) were examined using the LPS(0.3 μg·mL−1)-stimulated RAW264.7 macrophage model. The levels of NO, ROS, and iNOS were examined to analyze the anti-inflammatory activity of POL. Additionally, the levels of extracellular inflammation-related cytokines and chemokines were measured using quantibody array. The KEGG pathway analysis was performed to examine the anti-inflammatory mechanism of POL. The levels of NO in the POL-pretreated group were significantly downregulated when compared with those in the PS-E-pretreated, PS-F-pretreated, and PS-XLIX-pretreated groups. POL significantly inhibited the changes of iNOS, ROS, and inflammatory factors caused by LPS stimulation (p < 0.001). The expression levels of IL21 and GM-CSF were examined using qPCR, while those of JAK-STAT signaling pathway-related proteins in the LPS-stimulated RAW264.7 macrophages were analyzed using western blotting. POL significantly downregulated the expression of IL-21 and GM-CSF. The anti-inflammatory mechanism of POL is mediated through the JAK-STAT pathway. Thus, this study demonstrated that POL is an anti-inflammatory component of PJ and elucidated its mechanism.</abstract><cop>Japan</cop><pub>Elsevier B.V</pub><pmid>34384566</pmid><doi>10.1016/j.jphs.2021.06.010</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Anti-Inflammatory Agents Cytokines - genetics Cytokines - metabolism Down-Regulation - drug effects Drugs, Chinese Herbal - pharmacology Gene Expression - drug effects Glycosides - pharmacology IL21 Inflammation - etiology Inflammation - genetics Inflammation Mediators - metabolism Inflammation modulation Interleukins - genetics Interleukins - metabolism Lipopolysaccharides - adverse effects Mice Nitric Oxide - genetics Nitric Oxide - metabolism Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type II - metabolism Polygala - chemistry Polygala japonica Houtt Polygalaxanthone III Quantibody array RAW 264.7 Cells Reactive Oxygen Species - metabolism Signal Transduction - drug effects Xanthones - pharmacology |
| title | Polygalaxanthone III downregulates inflammation in the lipopolysaccharide-stimulated RAW264.7 macrophages: A quantibody array analysis |
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