Pinus densiflora needle supercritical fluid extract suppresses the expression of pro-inflammatory mediators iNOS, IL-6 and IL-1β, and activation of inflammatory STAT1 and STAT3 signaling proteins in bacterial lipopolysaccharide-challenged murine macrophages
Background Regulation of a persistently-activated inflammatory response in macrophages is an important target for treatment of various chronic diseases. Pine needle extracts are well known to have potent immunomodulatory effects. The current study was designed to evaluate the effects of Pinus densif...
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| Veröffentlicht in: | Daru 2017-08, Vol.25 (1), p.18, Article 18 |
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| description | Background
Regulation of a persistently-activated inflammatory response in macrophages is an important target for treatment of various chronic diseases. Pine needle extracts are well known to have potent immunomodulatory effects. The current study was designed to evaluate the effects of
Pinus densiflora
needle supercritical fluid extract (PDN-SCFE) on bacterial lipopolysaccharide (LPS)-induced inflammatory response in RAW 264.7 murine macrophages.
Methods
Cytotoxic effect of PDN-SCFE was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The levels of nitric oxide (NO) and the corresponding enzyme, inducible nitric oxide synthase (iNOS), were quantified by Griess and immunoblotting methods, respectively. The levels of cytokines were quantified using commercial ELISA kits. Quantitative real-time PCR (qRT-PCR) analysis was performed to assess the mRNA expression of iNOS and cytokines. To elucidate the mechanism of action, the involvement of nuclear transcription factor-kappa B (NFκB), mitogen activated protein kinases (MAPKs) and Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathways were examined by an immunoblotting method. In addition, the cellular localization of NFκB was analyzed by immunofluorescence staining.
Results
MTT assay results indicated that PDN-SCFE is non-toxic to RAW 264.7 cells up to a maximum assayed concentration of 40 μg/mL. The PDN-SCFE exhibited a concentration-dependent inhibitory effect on LPS-induced NO production by down regulating the expression of iNOS. In addition, the extract suppressed the LPS-induced expression of interleukin-6 (IL-6) and interleukin-1β (IL-1β) but not tumour necrosis factor-α (TNFα). Mechanistic studies revealed that PDN-SCFE does not influence the NFκB and MAPK pathways. However, it showed a significant inhibitory effect on LPS-induced activation of STAT1 and STAT3 proteins in macrophages.
Conclusion
The present findings revealed that the anti-inflammatory activity of PDN-SCFE in LPS-challenged RAW 264.7 macrophages is probably caused by the suppression of the JAK-STAT signaling pathway.
Graphical Abstract |
| doi_str_mv | 10.1186/s40199-017-0184-y |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5544993</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>28778215</sourcerecordid><originalsourceid>FETCH-LOGICAL-c357y-455797708aa462e1fe66ad770e8395915716f81a7023c080dc8cde5cf2b06b853</originalsourceid><addsrcrecordid>eNp9Uttu1DAQDRWIlsIH8IL8AQ3YSZw4L0hVBaXSiiJ1eba89mR3KseO7KRqfosP4Zvq7JaqfeHBmuO5nBkdnSz7yOhnxkT9JVaUtW1OWZOeqPL5KDspKBV5UZTs9TN8nL2L8ZbSUlR18TY7LkTTiILxk1dHv9BNkRhwETvrgyIOwFggcRog6IAjamVJZyc0BO7HoPS41IYAMUIk4w5Sev9D74jvyBB8jq6zqu_V6MNMejC4oEjw5_XNGbla5TVRziyA_f1ztseJFu_U-MjxYv5mfb5m-6YFlSTi1imLbrusGgFdInZkkxggYLrV4uAHb-eotN6pgAbyFK0FtwVD-imgA9IrHfywU1uI77M3nbIRPjzG0-z392_rix_56vry6uJ8leuSN3Necd60TUOFUklEYB3UtTIpAaJsect4w-pOMNXQotRUUKOFNsB1V2xovRG8PM2-HniHaZM00eCSmlYOAXsVZukVypcVhzu59XeS86pq2zIRsANBOj3GAN3TLKNyMYQ8GEImQ8jFEHJOM5-eL32a-OeA1FAcGmIqJYWCvPVTSALH_7A-AAYOyYY</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Pinus densiflora needle supercritical fluid extract suppresses the expression of pro-inflammatory mediators iNOS, IL-6 and IL-1β, and activation of inflammatory STAT1 and STAT3 signaling proteins in bacterial lipopolysaccharide-challenged murine macrophages</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>Free Full-Text Journals in Chemistry</source><creator>Venkatesan, Thamizhiniyan ; Choi, Young-Woong ; Lee, Jennifer ; Kim, Young-Kyoon</creator><creatorcontrib>Venkatesan, Thamizhiniyan ; Choi, Young-Woong ; Lee, Jennifer ; Kim, Young-Kyoon</creatorcontrib><description>Background
Regulation of a persistently-activated inflammatory response in macrophages is an important target for treatment of various chronic diseases. Pine needle extracts are well known to have potent immunomodulatory effects. The current study was designed to evaluate the effects of
Pinus densiflora
needle supercritical fluid extract (PDN-SCFE) on bacterial lipopolysaccharide (LPS)-induced inflammatory response in RAW 264.7 murine macrophages.
Methods
Cytotoxic effect of PDN-SCFE was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The levels of nitric oxide (NO) and the corresponding enzyme, inducible nitric oxide synthase (iNOS), were quantified by Griess and immunoblotting methods, respectively. The levels of cytokines were quantified using commercial ELISA kits. Quantitative real-time PCR (qRT-PCR) analysis was performed to assess the mRNA expression of iNOS and cytokines. To elucidate the mechanism of action, the involvement of nuclear transcription factor-kappa B (NFκB), mitogen activated protein kinases (MAPKs) and Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathways were examined by an immunoblotting method. In addition, the cellular localization of NFκB was analyzed by immunofluorescence staining.
Results
MTT assay results indicated that PDN-SCFE is non-toxic to RAW 264.7 cells up to a maximum assayed concentration of 40 μg/mL. The PDN-SCFE exhibited a concentration-dependent inhibitory effect on LPS-induced NO production by down regulating the expression of iNOS. In addition, the extract suppressed the LPS-induced expression of interleukin-6 (IL-6) and interleukin-1β (IL-1β) but not tumour necrosis factor-α (TNFα). Mechanistic studies revealed that PDN-SCFE does not influence the NFκB and MAPK pathways. However, it showed a significant inhibitory effect on LPS-induced activation of STAT1 and STAT3 proteins in macrophages.
Conclusion
The present findings revealed that the anti-inflammatory activity of PDN-SCFE in LPS-challenged RAW 264.7 macrophages is probably caused by the suppression of the JAK-STAT signaling pathway.
Graphical Abstract</description><identifier>ISSN: 2008-2231</identifier><identifier>ISSN: 1560-8115</identifier><identifier>EISSN: 2008-2231</identifier><identifier>DOI: 10.1186/s40199-017-0184-y</identifier><identifier>PMID: 28778215</identifier><language>eng</language><publisher>London: BioMed Central</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Blotting, Western ; Inflammation - drug therapy ; Interleukin-18 - antagonists & inhibitors ; Interleukin-6 - antagonists & inhibitors ; Lipopolysaccharides - pharmacology ; Macrophages - drug effects ; Medicinal Chemistry ; Mice ; Microscopy, Fluorescence ; Nitric Oxide Synthase Type II - antagonists & inhibitors ; Pharmaceutical Sciences/Technology ; Pharmacology/Toxicology ; Pinus - chemistry ; Plant Extracts - pharmacology ; Plant Leaves - chemistry ; RAW 264.7 Cells ; Real-Time Polymerase Chain Reaction ; Research Article ; STAT1 Transcription Factor - antagonists & inhibitors ; STAT3 Transcription Factor - antagonists & inhibitors</subject><ispartof>Daru, 2017-08, Vol.25 (1), p.18, Article 18</ispartof><rights>The Author(s). 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c357y-455797708aa462e1fe66ad770e8395915716f81a7023c080dc8cde5cf2b06b853</citedby><cites>FETCH-LOGICAL-c357y-455797708aa462e1fe66ad770e8395915716f81a7023c080dc8cde5cf2b06b853</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/PMC5544993/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5544993/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28778215$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Venkatesan, Thamizhiniyan</creatorcontrib><creatorcontrib>Choi, Young-Woong</creatorcontrib><creatorcontrib>Lee, Jennifer</creatorcontrib><creatorcontrib>Kim, Young-Kyoon</creatorcontrib><title>Pinus densiflora needle supercritical fluid extract suppresses the expression of pro-inflammatory mediators iNOS, IL-6 and IL-1β, and activation of inflammatory STAT1 and STAT3 signaling proteins in bacterial lipopolysaccharide-challenged murine macrophages</title><title>Daru</title><addtitle>DARU J Pharm Sci</addtitle><addtitle>Daru</addtitle><description>Background
Regulation of a persistently-activated inflammatory response in macrophages is an important target for treatment of various chronic diseases. Pine needle extracts are well known to have potent immunomodulatory effects. The current study was designed to evaluate the effects of
Pinus densiflora
needle supercritical fluid extract (PDN-SCFE) on bacterial lipopolysaccharide (LPS)-induced inflammatory response in RAW 264.7 murine macrophages.
Methods
Cytotoxic effect of PDN-SCFE was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The levels of nitric oxide (NO) and the corresponding enzyme, inducible nitric oxide synthase (iNOS), were quantified by Griess and immunoblotting methods, respectively. The levels of cytokines were quantified using commercial ELISA kits. Quantitative real-time PCR (qRT-PCR) analysis was performed to assess the mRNA expression of iNOS and cytokines. To elucidate the mechanism of action, the involvement of nuclear transcription factor-kappa B (NFκB), mitogen activated protein kinases (MAPKs) and Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathways were examined by an immunoblotting method. In addition, the cellular localization of NFκB was analyzed by immunofluorescence staining.
Results
MTT assay results indicated that PDN-SCFE is non-toxic to RAW 264.7 cells up to a maximum assayed concentration of 40 μg/mL. The PDN-SCFE exhibited a concentration-dependent inhibitory effect on LPS-induced NO production by down regulating the expression of iNOS. In addition, the extract suppressed the LPS-induced expression of interleukin-6 (IL-6) and interleukin-1β (IL-1β) but not tumour necrosis factor-α (TNFα). Mechanistic studies revealed that PDN-SCFE does not influence the NFκB and MAPK pathways. However, it showed a significant inhibitory effect on LPS-induced activation of STAT1 and STAT3 proteins in macrophages.
Conclusion
The present findings revealed that the anti-inflammatory activity of PDN-SCFE in LPS-challenged RAW 264.7 macrophages is probably caused by the suppression of the JAK-STAT signaling pathway.
Graphical Abstract</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blotting, Western</subject><subject>Inflammation - drug therapy</subject><subject>Interleukin-18 - antagonists & inhibitors</subject><subject>Interleukin-6 - antagonists & inhibitors</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Macrophages - drug effects</subject><subject>Medicinal Chemistry</subject><subject>Mice</subject><subject>Microscopy, Fluorescence</subject><subject>Nitric Oxide Synthase Type II - antagonists & inhibitors</subject><subject>Pharmaceutical Sciences/Technology</subject><subject>Pharmacology/Toxicology</subject><subject>Pinus - chemistry</subject><subject>Plant Extracts - pharmacology</subject><subject>Plant Leaves - chemistry</subject><subject>RAW 264.7 Cells</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Research Article</subject><subject>STAT1 Transcription Factor - antagonists & inhibitors</subject><subject>STAT3 Transcription Factor - antagonists & inhibitors</subject><issn>2008-2231</issn><issn>1560-8115</issn><issn>2008-2231</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><recordid>eNp9Uttu1DAQDRWIlsIH8IL8AQ3YSZw4L0hVBaXSiiJ1eba89mR3KseO7KRqfosP4Zvq7JaqfeHBmuO5nBkdnSz7yOhnxkT9JVaUtW1OWZOeqPL5KDspKBV5UZTs9TN8nL2L8ZbSUlR18TY7LkTTiILxk1dHv9BNkRhwETvrgyIOwFggcRog6IAjamVJZyc0BO7HoPS41IYAMUIk4w5Sev9D74jvyBB8jq6zqu_V6MNMejC4oEjw5_XNGbla5TVRziyA_f1ztseJFu_U-MjxYv5mfb5m-6YFlSTi1imLbrusGgFdInZkkxggYLrV4uAHb-eotN6pgAbyFK0FtwVD-imgA9IrHfywU1uI77M3nbIRPjzG0-z392_rix_56vry6uJ8leuSN3Necd60TUOFUklEYB3UtTIpAaJsect4w-pOMNXQotRUUKOFNsB1V2xovRG8PM2-HniHaZM00eCSmlYOAXsVZukVypcVhzu59XeS86pq2zIRsANBOj3GAN3TLKNyMYQ8GEImQ8jFEHJOM5-eL32a-OeA1FAcGmIqJYWCvPVTSALH_7A-AAYOyYY</recordid><startdate>20170804</startdate><enddate>20170804</enddate><creator>Venkatesan, Thamizhiniyan</creator><creator>Choi, Young-Woong</creator><creator>Lee, Jennifer</creator><creator>Kim, Young-Kyoon</creator><general>BioMed Central</general><scope>C6C</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>5PM</scope></search><sort><creationdate>20170804</creationdate><title>Pinus densiflora needle supercritical fluid extract suppresses the expression of pro-inflammatory mediators iNOS, IL-6 and IL-1β, and activation of inflammatory STAT1 and STAT3 signaling proteins in bacterial lipopolysaccharide-challenged murine macrophages</title><author>Venkatesan, Thamizhiniyan ; Choi, Young-Woong ; Lee, Jennifer ; Kim, Young-Kyoon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c357y-455797708aa462e1fe66ad770e8395915716f81a7023c080dc8cde5cf2b06b853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blotting, Western</topic><topic>Inflammation - drug therapy</topic><topic>Interleukin-18 - antagonists & inhibitors</topic><topic>Interleukin-6 - antagonists & inhibitors</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Macrophages - drug effects</topic><topic>Medicinal Chemistry</topic><topic>Mice</topic><topic>Microscopy, Fluorescence</topic><topic>Nitric Oxide Synthase Type II - antagonists & inhibitors</topic><topic>Pharmaceutical Sciences/Technology</topic><topic>Pharmacology/Toxicology</topic><topic>Pinus - chemistry</topic><topic>Plant Extracts - pharmacology</topic><topic>Plant Leaves - chemistry</topic><topic>RAW 264.7 Cells</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Research Article</topic><topic>STAT1 Transcription Factor - antagonists & inhibitors</topic><topic>STAT3 Transcription Factor - antagonists & inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Venkatesan, Thamizhiniyan</creatorcontrib><creatorcontrib>Choi, Young-Woong</creatorcontrib><creatorcontrib>Lee, Jennifer</creatorcontrib><creatorcontrib>Kim, Young-Kyoon</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Daru</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Venkatesan, Thamizhiniyan</au><au>Choi, Young-Woong</au><au>Lee, Jennifer</au><au>Kim, Young-Kyoon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pinus densiflora needle supercritical fluid extract suppresses the expression of pro-inflammatory mediators iNOS, IL-6 and IL-1β, and activation of inflammatory STAT1 and STAT3 signaling proteins in bacterial lipopolysaccharide-challenged murine macrophages</atitle><jtitle>Daru</jtitle><stitle>DARU J Pharm Sci</stitle><addtitle>Daru</addtitle><date>2017-08-04</date><risdate>2017</risdate><volume>25</volume><issue>1</issue><spage>18</spage><pages>18-</pages><artnum>18</artnum><issn>2008-2231</issn><issn>1560-8115</issn><eissn>2008-2231</eissn><abstract>Background
Regulation of a persistently-activated inflammatory response in macrophages is an important target for treatment of various chronic diseases. Pine needle extracts are well known to have potent immunomodulatory effects. The current study was designed to evaluate the effects of
Pinus densiflora
needle supercritical fluid extract (PDN-SCFE) on bacterial lipopolysaccharide (LPS)-induced inflammatory response in RAW 264.7 murine macrophages.
Methods
Cytotoxic effect of PDN-SCFE was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The levels of nitric oxide (NO) and the corresponding enzyme, inducible nitric oxide synthase (iNOS), were quantified by Griess and immunoblotting methods, respectively. The levels of cytokines were quantified using commercial ELISA kits. Quantitative real-time PCR (qRT-PCR) analysis was performed to assess the mRNA expression of iNOS and cytokines. To elucidate the mechanism of action, the involvement of nuclear transcription factor-kappa B (NFκB), mitogen activated protein kinases (MAPKs) and Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathways were examined by an immunoblotting method. In addition, the cellular localization of NFκB was analyzed by immunofluorescence staining.
Results
MTT assay results indicated that PDN-SCFE is non-toxic to RAW 264.7 cells up to a maximum assayed concentration of 40 μg/mL. The PDN-SCFE exhibited a concentration-dependent inhibitory effect on LPS-induced NO production by down regulating the expression of iNOS. In addition, the extract suppressed the LPS-induced expression of interleukin-6 (IL-6) and interleukin-1β (IL-1β) but not tumour necrosis factor-α (TNFα). Mechanistic studies revealed that PDN-SCFE does not influence the NFκB and MAPK pathways. However, it showed a significant inhibitory effect on LPS-induced activation of STAT1 and STAT3 proteins in macrophages.
Conclusion
The present findings revealed that the anti-inflammatory activity of PDN-SCFE in LPS-challenged RAW 264.7 macrophages is probably caused by the suppression of the JAK-STAT signaling pathway.
Graphical Abstract</abstract><cop>London</cop><pub>BioMed Central</pub><pmid>28778215</pmid><doi>10.1186/s40199-017-0184-y</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Springer Nature - Complete Springer Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | Animals Biomedical and Life Sciences Biomedicine Blotting, Western Inflammation - drug therapy Interleukin-18 - antagonists & inhibitors Interleukin-6 - antagonists & inhibitors Lipopolysaccharides - pharmacology Macrophages - drug effects Medicinal Chemistry Mice Microscopy, Fluorescence Nitric Oxide Synthase Type II - antagonists & inhibitors Pharmaceutical Sciences/Technology Pharmacology/Toxicology Pinus - chemistry Plant Extracts - pharmacology Plant Leaves - chemistry RAW 264.7 Cells Real-Time Polymerase Chain Reaction Research Article STAT1 Transcription Factor - antagonists & inhibitors STAT3 Transcription Factor - antagonists & inhibitors |
| title | Pinus densiflora needle supercritical fluid extract suppresses the expression of pro-inflammatory mediators iNOS, IL-6 and IL-1β, and activation of inflammatory STAT1 and STAT3 signaling proteins in bacterial lipopolysaccharide-challenged murine macrophages |
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