Silymarin Suppresses Cellular Inflammation By Inducing Reparative Stress Signaling
Silymarin, a characterized extract of the seeds of milk thistle (Silybum marianum), suppresses cellular inflammation. To define how this occurs, transcriptional profiling, metabolomics, and signaling studies were performed in human liver and T cell lines. Cellular stress and metabolic pathways were...
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creator | Lovelace, Erica S Wagoner, Jessica MacDonald, James Bammler, Theo Bruckner, Jacob Brownell, Jessica Beyer, Richard P Zink, Erika M Kim, Young-Mo Kyle, Jennifer E Webb-Robertson, Bobbie-Jo M Waters, Katrina M Metz, Thomas O Farin, Federico Oberlies, Nicholas H Polyak, Stephen J |
description | Silymarin, a characterized extract of the seeds of milk thistle (Silybum marianum), suppresses cellular inflammation. To define how this occurs, transcriptional profiling, metabolomics, and signaling studies were performed in human liver and T cell lines. Cellular stress and metabolic pathways were modulated within 4 h of silymarin treatment: activation of Activating Transcription Factor 4 (ATF-4) and adenosine monophosphate protein kinase (AMPK) and inhibition of mammalian target of rapamycin (mTOR) signaling, the latter being associated with induction of DNA-damage-inducible transcript 4 (DDIT4). Metabolomics analyses revealed silymarin suppression of glycolytic, tricarboxylic acid (TCA) cycle, and amino acid metabolism. Anti-inflammatory effects arose with prolonged (i.e., 24 h) silymarin exposure, with suppression of multiple pro-inflammatory mRNAs and signaling pathways including nuclear factor kappa B (NF-κB) and forkhead box O (FOXO). Studies with murine knock out cells revealed that silymarin inhibition of both mTOR and NF-κB was partially AMPK dependent, whereas silymarin inhibition of mTOR required DDIT4. Other natural products induced similar stress responses, which correlated with their ability to suppress inflammation. Thus, natural products activate stress and repair responses that culminate in an anti-inflammatory cellular phenotype. Natural products like silymarin may be useful as tools to define how metabolic, stress, and repair pathways regulate cellular inflammation. |
doi_str_mv | 10.1021/acs.jnatprod.5b00288 |
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To define how this occurs, transcriptional profiling, metabolomics, and signaling studies were performed in human liver and T cell lines. Cellular stress and metabolic pathways were modulated within 4 h of silymarin treatment: activation of Activating Transcription Factor 4 (ATF-4) and adenosine monophosphate protein kinase (AMPK) and inhibition of mammalian target of rapamycin (mTOR) signaling, the latter being associated with induction of DNA-damage-inducible transcript 4 (DDIT4). Metabolomics analyses revealed silymarin suppression of glycolytic, tricarboxylic acid (TCA) cycle, and amino acid metabolism. Anti-inflammatory effects arose with prolonged (i.e., 24 h) silymarin exposure, with suppression of multiple pro-inflammatory mRNAs and signaling pathways including nuclear factor kappa B (NF-κB) and forkhead box O (FOXO). Studies with murine knock out cells revealed that silymarin inhibition of both mTOR and NF-κB was partially AMPK dependent, whereas silymarin inhibition of mTOR required DDIT4. Other natural products induced similar stress responses, which correlated with their ability to suppress inflammation. Thus, natural products activate stress and repair responses that culminate in an anti-inflammatory cellular phenotype. Natural products like silymarin may be useful as tools to define how metabolic, stress, and repair pathways regulate cellular inflammation.</description><identifier>ISSN: 0163-3864</identifier><identifier>ISSN: 1520-6025</identifier><identifier>EISSN: 1520-6025</identifier><identifier>DOI: 10.1021/acs.jnatprod.5b00288</identifier><identifier>PMID: 26186142</identifier><language>eng</language><publisher>United States: American Chemical Society and American Society of Pharmacognosy</publisher><subject>adenosine monophosphate ; amino acid metabolism ; AMP-Activated Protein Kinases - drug effects ; Animals ; anti-inflammatory activity ; Anti-Inflammatory Agents - chemistry ; Anti-Inflammatory Agents - pharmacology ; Antioxidants - pharmacology ; Citric Acid Cycle - drug effects ; Environmental Molecular Sciences Laboratory ; Forkhead Transcription Factors - drug effects ; glycolysis ; Humans ; inflammation ; Inflammation - drug therapy ; Inflammation - metabolism ; Jurkat Cells ; liver ; Liver - metabolism ; messenger RNA ; metabolomics ; Mice ; Molecular Structure ; NF-kappa B - antagonists & inhibitors ; NF-kappa B - drug effects ; Nitric Oxide Synthase Type II ; phenotype ; protein kinases ; rapamycin ; seeds ; signal transduction ; Signal Transduction - drug effects ; Silybum marianum ; Silybum marianum - chemistry ; silymarin ; Silymarin - chemistry ; Silymarin - pharmacology ; stress response ; T-lymphocytes ; T-Lymphocytes - metabolism ; transcription (genetics) ; transcription factor NF-kappa B ; tricarboxylic acid cycle</subject><ispartof>Journal of Natural Products, 78(8):1990-2000, 2015-08, Vol.78 (8), p.1990-2000</ispartof><rights>Copyright © American Chemical Society and American Society of Pharmacognosy</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a509t-794a07a8a82851338a1df61c58009037f7bbf142e90be25be6e89ef08fc528ae3</citedby><cites>FETCH-LOGICAL-a509t-794a07a8a82851338a1df61c58009037f7bbf142e90be25be6e89ef08fc528ae3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://pubs.acs.org/doi/pdf/10.1021/acs.jnatprod.5b00288$$EPDF$$P50$$Gacs$$H</linktopdf><linktohtml>$$Uhttps://pubs.acs.org/doi/10.1021/acs.jnatprod.5b00288$$EHTML$$P50$$Gacs$$H</linktohtml><link.rule.ids>230,314,776,780,881,2752,27053,27901,27902,56713,56763</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26186142$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/1214891$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Lovelace, Erica S</creatorcontrib><creatorcontrib>Wagoner, Jessica</creatorcontrib><creatorcontrib>MacDonald, James</creatorcontrib><creatorcontrib>Bammler, Theo</creatorcontrib><creatorcontrib>Bruckner, Jacob</creatorcontrib><creatorcontrib>Brownell, Jessica</creatorcontrib><creatorcontrib>Beyer, Richard P</creatorcontrib><creatorcontrib>Zink, Erika M</creatorcontrib><creatorcontrib>Kim, Young-Mo</creatorcontrib><creatorcontrib>Kyle, Jennifer E</creatorcontrib><creatorcontrib>Webb-Robertson, Bobbie-Jo M</creatorcontrib><creatorcontrib>Waters, Katrina M</creatorcontrib><creatorcontrib>Metz, Thomas O</creatorcontrib><creatorcontrib>Farin, Federico</creatorcontrib><creatorcontrib>Oberlies, Nicholas H</creatorcontrib><creatorcontrib>Polyak, Stephen J</creatorcontrib><creatorcontrib>Pacific Northwest National Laboratory (PNNL), Richland, WA (US), Environmental Molecular Sciences Laboratory (EMSL)</creatorcontrib><title>Silymarin Suppresses Cellular Inflammation By Inducing Reparative Stress Signaling</title><title>Journal of Natural Products, 78(8):1990-2000</title><addtitle>J. Nat. Prod</addtitle><description>Silymarin, a characterized extract of the seeds of milk thistle (Silybum marianum), suppresses cellular inflammation. To define how this occurs, transcriptional profiling, metabolomics, and signaling studies were performed in human liver and T cell lines. Cellular stress and metabolic pathways were modulated within 4 h of silymarin treatment: activation of Activating Transcription Factor 4 (ATF-4) and adenosine monophosphate protein kinase (AMPK) and inhibition of mammalian target of rapamycin (mTOR) signaling, the latter being associated with induction of DNA-damage-inducible transcript 4 (DDIT4). Metabolomics analyses revealed silymarin suppression of glycolytic, tricarboxylic acid (TCA) cycle, and amino acid metabolism. Anti-inflammatory effects arose with prolonged (i.e., 24 h) silymarin exposure, with suppression of multiple pro-inflammatory mRNAs and signaling pathways including nuclear factor kappa B (NF-κB) and forkhead box O (FOXO). Studies with murine knock out cells revealed that silymarin inhibition of both mTOR and NF-κB was partially AMPK dependent, whereas silymarin inhibition of mTOR required DDIT4. Other natural products induced similar stress responses, which correlated with their ability to suppress inflammation. Thus, natural products activate stress and repair responses that culminate in an anti-inflammatory cellular phenotype. Natural products like silymarin may be useful as tools to define how metabolic, stress, and repair pathways regulate cellular inflammation.</description><subject>adenosine monophosphate</subject><subject>amino acid metabolism</subject><subject>AMP-Activated Protein Kinases - drug effects</subject><subject>Animals</subject><subject>anti-inflammatory activity</subject><subject>Anti-Inflammatory Agents - chemistry</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Antioxidants - pharmacology</subject><subject>Citric Acid Cycle - drug effects</subject><subject>Environmental Molecular Sciences Laboratory</subject><subject>Forkhead Transcription Factors - drug effects</subject><subject>glycolysis</subject><subject>Humans</subject><subject>inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - metabolism</subject><subject>Jurkat Cells</subject><subject>liver</subject><subject>Liver - metabolism</subject><subject>messenger RNA</subject><subject>metabolomics</subject><subject>Mice</subject><subject>Molecular Structure</subject><subject>NF-kappa B - antagonists & inhibitors</subject><subject>NF-kappa B - drug effects</subject><subject>Nitric Oxide Synthase Type II</subject><subject>phenotype</subject><subject>protein kinases</subject><subject>rapamycin</subject><subject>seeds</subject><subject>signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Silybum marianum</subject><subject>Silybum marianum - chemistry</subject><subject>silymarin</subject><subject>Silymarin - chemistry</subject><subject>Silymarin - pharmacology</subject><subject>stress response</subject><subject>T-lymphocytes</subject><subject>T-Lymphocytes - metabolism</subject><subject>transcription (genetics)</subject><subject>transcription factor NF-kappa B</subject><subject>tricarboxylic acid cycle</subject><issn>0163-3864</issn><issn>1520-6025</issn><issn>1520-6025</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UU2P0zAQtRCILQv_AKGIE5eUsWMnzgUJKj5WWglpC2dr4k66XiV2sJOV-u9xaXcFF07WeN57M_MeY685rDkI_h5tWt95nKcYdmvVAQitn7AVVwLKGoR6ylbA66qsdC0v2IuU7gCgglY9Zxei5rrmUqzYzdYNhxGj88V2maZIKVEqNjQMy4CxuPL9gOOIswu--HTI9W6xzu-LG5ow5u97KrbzkVVs3d7jkHsv2bMeh0Svzu8l-_nl84_Nt_L6-9erzcfrEhW0c9m0EqFBjVpoxatKI9_1NbdKA7RQNX3TdX3ekVroSKiOatIt9aB7q4RGqi7Zh5PutHQj7Sz5OeJgpujyPQcT0Jl_O97dmn24N7I5-iCzwNuTQEizM8m6meytDd6TnQ0XXOqWZ9C785QYfi2UZjO6ZLM_6CksyYjsqpQVQJOh8gS1MaQUqX_chYM5ZmZyZuYhM3POLNPe_H3HI-khpAyAE-APPSwx-5z-r_kbgIWn_Q</recordid><startdate>20150828</startdate><enddate>20150828</enddate><creator>Lovelace, Erica S</creator><creator>Wagoner, Jessica</creator><creator>MacDonald, James</creator><creator>Bammler, Theo</creator><creator>Bruckner, Jacob</creator><creator>Brownell, Jessica</creator><creator>Beyer, Richard P</creator><creator>Zink, Erika M</creator><creator>Kim, Young-Mo</creator><creator>Kyle, Jennifer E</creator><creator>Webb-Robertson, Bobbie-Jo M</creator><creator>Waters, Katrina M</creator><creator>Metz, Thomas O</creator><creator>Farin, Federico</creator><creator>Oberlies, Nicholas H</creator><creator>Polyak, Stephen J</creator><general>American Chemical Society and American Society of Pharmacognosy</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>7S9</scope><scope>L.6</scope><scope>OTOTI</scope><scope>5PM</scope></search><sort><creationdate>20150828</creationdate><title>Silymarin Suppresses Cellular Inflammation By Inducing Reparative Stress Signaling</title><author>Lovelace, Erica S ; Wagoner, Jessica ; MacDonald, James ; Bammler, Theo ; Bruckner, Jacob ; Brownell, Jessica ; Beyer, Richard P ; Zink, Erika M ; Kim, Young-Mo ; Kyle, Jennifer E ; Webb-Robertson, Bobbie-Jo M ; Waters, Katrina M ; Metz, Thomas O ; Farin, Federico ; Oberlies, Nicholas H ; Polyak, Stephen J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a509t-794a07a8a82851338a1df61c58009037f7bbf142e90be25be6e89ef08fc528ae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>adenosine monophosphate</topic><topic>amino acid metabolism</topic><topic>AMP-Activated Protein Kinases - drug effects</topic><topic>Animals</topic><topic>anti-inflammatory activity</topic><topic>Anti-Inflammatory Agents - chemistry</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Antioxidants - pharmacology</topic><topic>Citric Acid Cycle - drug effects</topic><topic>Environmental Molecular Sciences Laboratory</topic><topic>Forkhead Transcription Factors - drug effects</topic><topic>glycolysis</topic><topic>Humans</topic><topic>inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - metabolism</topic><topic>Jurkat Cells</topic><topic>liver</topic><topic>Liver - metabolism</topic><topic>messenger RNA</topic><topic>metabolomics</topic><topic>Mice</topic><topic>Molecular Structure</topic><topic>NF-kappa B - antagonists & inhibitors</topic><topic>NF-kappa B - drug effects</topic><topic>Nitric Oxide Synthase Type II</topic><topic>phenotype</topic><topic>protein kinases</topic><topic>rapamycin</topic><topic>seeds</topic><topic>signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Silybum marianum</topic><topic>Silybum marianum - chemistry</topic><topic>silymarin</topic><topic>Silymarin - chemistry</topic><topic>Silymarin - pharmacology</topic><topic>stress response</topic><topic>T-lymphocytes</topic><topic>T-Lymphocytes - metabolism</topic><topic>transcription (genetics)</topic><topic>transcription factor NF-kappa B</topic><topic>tricarboxylic acid cycle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lovelace, Erica S</creatorcontrib><creatorcontrib>Wagoner, Jessica</creatorcontrib><creatorcontrib>MacDonald, James</creatorcontrib><creatorcontrib>Bammler, Theo</creatorcontrib><creatorcontrib>Bruckner, Jacob</creatorcontrib><creatorcontrib>Brownell, Jessica</creatorcontrib><creatorcontrib>Beyer, Richard P</creatorcontrib><creatorcontrib>Zink, Erika M</creatorcontrib><creatorcontrib>Kim, Young-Mo</creatorcontrib><creatorcontrib>Kyle, Jennifer E</creatorcontrib><creatorcontrib>Webb-Robertson, Bobbie-Jo M</creatorcontrib><creatorcontrib>Waters, Katrina M</creatorcontrib><creatorcontrib>Metz, Thomas O</creatorcontrib><creatorcontrib>Farin, Federico</creatorcontrib><creatorcontrib>Oberlies, Nicholas H</creatorcontrib><creatorcontrib>Polyak, Stephen J</creatorcontrib><creatorcontrib>Pacific Northwest National Laboratory (PNNL), Richland, WA (US), Environmental Molecular Sciences Laboratory (EMSL)</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>OSTI.GOV</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of Natural Products, 78(8):1990-2000</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lovelace, Erica S</au><au>Wagoner, Jessica</au><au>MacDonald, James</au><au>Bammler, Theo</au><au>Bruckner, Jacob</au><au>Brownell, Jessica</au><au>Beyer, Richard P</au><au>Zink, Erika M</au><au>Kim, Young-Mo</au><au>Kyle, Jennifer E</au><au>Webb-Robertson, Bobbie-Jo M</au><au>Waters, Katrina M</au><au>Metz, Thomas O</au><au>Farin, Federico</au><au>Oberlies, Nicholas H</au><au>Polyak, Stephen J</au><aucorp>Pacific Northwest National Laboratory (PNNL), Richland, WA (US), Environmental Molecular Sciences Laboratory (EMSL)</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Silymarin Suppresses Cellular Inflammation By Inducing Reparative Stress Signaling</atitle><jtitle>Journal of Natural Products, 78(8):1990-2000</jtitle><addtitle>J. Nat. Prod</addtitle><date>2015-08-28</date><risdate>2015</risdate><volume>78</volume><issue>8</issue><spage>1990</spage><epage>2000</epage><pages>1990-2000</pages><issn>0163-3864</issn><issn>1520-6025</issn><eissn>1520-6025</eissn><abstract>Silymarin, a characterized extract of the seeds of milk thistle (Silybum marianum), suppresses cellular inflammation. To define how this occurs, transcriptional profiling, metabolomics, and signaling studies were performed in human liver and T cell lines. Cellular stress and metabolic pathways were modulated within 4 h of silymarin treatment: activation of Activating Transcription Factor 4 (ATF-4) and adenosine monophosphate protein kinase (AMPK) and inhibition of mammalian target of rapamycin (mTOR) signaling, the latter being associated with induction of DNA-damage-inducible transcript 4 (DDIT4). Metabolomics analyses revealed silymarin suppression of glycolytic, tricarboxylic acid (TCA) cycle, and amino acid metabolism. Anti-inflammatory effects arose with prolonged (i.e., 24 h) silymarin exposure, with suppression of multiple pro-inflammatory mRNAs and signaling pathways including nuclear factor kappa B (NF-κB) and forkhead box O (FOXO). Studies with murine knock out cells revealed that silymarin inhibition of both mTOR and NF-κB was partially AMPK dependent, whereas silymarin inhibition of mTOR required DDIT4. Other natural products induced similar stress responses, which correlated with their ability to suppress inflammation. Thus, natural products activate stress and repair responses that culminate in an anti-inflammatory cellular phenotype. Natural products like silymarin may be useful as tools to define how metabolic, stress, and repair pathways regulate cellular inflammation.</abstract><cop>United States</cop><pub>American Chemical Society and American Society of Pharmacognosy</pub><pmid>26186142</pmid><doi>10.1021/acs.jnatprod.5b00288</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | adenosine monophosphate amino acid metabolism AMP-Activated Protein Kinases - drug effects Animals anti-inflammatory activity Anti-Inflammatory Agents - chemistry Anti-Inflammatory Agents - pharmacology Antioxidants - pharmacology Citric Acid Cycle - drug effects Environmental Molecular Sciences Laboratory Forkhead Transcription Factors - drug effects glycolysis Humans inflammation Inflammation - drug therapy Inflammation - metabolism Jurkat Cells liver Liver - metabolism messenger RNA metabolomics Mice Molecular Structure NF-kappa B - antagonists & inhibitors NF-kappa B - drug effects Nitric Oxide Synthase Type II phenotype protein kinases rapamycin seeds signal transduction Signal Transduction - drug effects Silybum marianum Silybum marianum - chemistry silymarin Silymarin - chemistry Silymarin - pharmacology stress response T-lymphocytes T-Lymphocytes - metabolism transcription (genetics) transcription factor NF-kappa B tricarboxylic acid cycle |
title | Silymarin Suppresses Cellular Inflammation By Inducing Reparative Stress Signaling |
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