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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Veröffentlicht in:Journal of Natural Products, 78(8):1990-2000 78(8):1990-2000, 2015-08, Vol.78 (8), p.1990-2000
Hauptverfasser: 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
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container_end_page 2000
container_issue 8
container_start_page 1990
container_title Journal of Natural Products, 78(8):1990-2000
container_volume 78
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. 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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. 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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 &amp; 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source ACS Publications; MEDLINE
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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