Saturated long-chain fatty acids activate inflammatory signaling in astrocytes
J. Neurochem. (2012) 120, 1060–1071. This study describes the effects of long‐chain fatty acids on inflammatory signaling in cultured astrocytes. Data show that the saturated fatty acid palmitic acid, as well as lauric acid and stearic acid, trigger the release of TNFα and IL‐6 from astrocytes. Unsa...
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| description | J. Neurochem. (2012) 120, 1060–1071.
This study describes the effects of long‐chain fatty acids on inflammatory signaling in cultured astrocytes. Data show that the saturated fatty acid palmitic acid, as well as lauric acid and stearic acid, trigger the release of TNFα and IL‐6 from astrocytes. Unsaturated fatty acids were unable to induce cytokine release from cultured astrocytes. Furthermore, the effects of palmitic acid on cytokine release require Toll‐like receptor 4 rather than CD36 or Toll‐like receptor 2, and do not depend on palmitic acid metabolism to palmitoyl‐CoA. Inhibitor studies revealed that pharmacologic inhibition of p38 or p42/44 MAPK pathways prevents the pro‐inflammatory effects of palmitic acid, whereas JNK and PI3K inhibition does not affect cytokine release. Depletion of microglia from primary astrocyte cultures using the lysosomotropic agent l‐leucine methyl ester revealed that the ability of palmitic acid to trigger cytokine release is not dependent on the presence of microglia. Finally, data show that the essential ω‐3 fatty acid docosahexaenoic acid acts in a dose‐dependent manner to prevent the actions of palmitic acid on inflammatory signaling in astrocytes. Collectively, these data demonstrate the ability of saturated fatty acids to induce astrocyte inflammation in vitro. These data thus raise the possibility that high levels of circulating saturated fatty acids could cause reactive gliosis and brain inflammation in vivo, and could potentially participate in the reported adverse neurologic consequences of obesity and metabolic syndrome.
The good fat, the bad fat, and the brain
Obesity and metabolic syndrome detrimentally affect the brain through unknown mechanisms. This paper demonstrates the ability of saturated fatty acids to trigger cytokine release from cultured astrocytes, and the ability of ω‐3 unsaturated fatty acids to block cytokine release. These data suggest that circulating saturated fatty acids could cause brain inflammation and thus participate in the adverse neurologic consequences of metabolic syndrome |
| doi_str_mv | 10.1111/j.1471-4159.2012.07660.x |
| format | Article |
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This study describes the effects of long‐chain fatty acids on inflammatory signaling in cultured astrocytes. Data show that the saturated fatty acid palmitic acid, as well as lauric acid and stearic acid, trigger the release of TNFα and IL‐6 from astrocytes. Unsaturated fatty acids were unable to induce cytokine release from cultured astrocytes. Furthermore, the effects of palmitic acid on cytokine release require Toll‐like receptor 4 rather than CD36 or Toll‐like receptor 2, and do not depend on palmitic acid metabolism to palmitoyl‐CoA. Inhibitor studies revealed that pharmacologic inhibition of p38 or p42/44 MAPK pathways prevents the pro‐inflammatory effects of palmitic acid, whereas JNK and PI3K inhibition does not affect cytokine release. Depletion of microglia from primary astrocyte cultures using the lysosomotropic agent l‐leucine methyl ester revealed that the ability of palmitic acid to trigger cytokine release is not dependent on the presence of microglia. Finally, data show that the essential ω‐3 fatty acid docosahexaenoic acid acts in a dose‐dependent manner to prevent the actions of palmitic acid on inflammatory signaling in astrocytes. Collectively, these data demonstrate the ability of saturated fatty acids to induce astrocyte inflammation in vitro. These data thus raise the possibility that high levels of circulating saturated fatty acids could cause reactive gliosis and brain inflammation in vivo, and could potentially participate in the reported adverse neurologic consequences of obesity and metabolic syndrome.
The good fat, the bad fat, and the brain
Obesity and metabolic syndrome detrimentally affect the brain through unknown mechanisms. This paper demonstrates the ability of saturated fatty acids to trigger cytokine release from cultured astrocytes, and the ability of ω‐3 unsaturated fatty acids to block cytokine release. These data suggest that circulating saturated fatty acids could cause brain inflammation and thus participate in the adverse neurologic consequences of metabolic syndrome</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.2012.07660.x</identifier><identifier>PMID: 22248073</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Animals, Newborn ; Astrocytes ; Astrocytes - drug effects ; Biological and medical sciences ; Brain ; Brain - cytology ; brain inflammation ; c-Jun amino-terminal kinase ; CD36 antigen ; Cells ; Cells, Cultured ; Cytokines ; Cytokines - metabolism ; Data processing ; Docosahexaenoic acid ; Dose-Response Relationship, Drug ; Drug Interactions ; dyslipidemia ; Enzyme Inhibitors - pharmacology ; Enzyme-Linked Immunosorbent Assay ; Fatty acids ; Fatty Acids - metabolism ; Fatty Acids - pharmacology ; Female ; Gene Expression Regulation - drug effects ; Gliosis ; Inflammation ; Male ; MAP kinase ; Medical sciences ; Metabolic diseases ; Metabolic disorders ; Microglia ; Miscellaneous ; Neurochemistry ; Obesity ; Oleic Acid - pharmacology ; Other metabolic disorders ; Palmitic acid ; Palmitic Acid - pharmacology ; Rats ; Rats, Sprague-Dawley ; reactive gliosis ; Signal transduction ; Signal Transduction - drug effects ; Stearic acid ; Toll-Like Receptor 2 - metabolism ; Toll-Like Receptor 4 - metabolism ; Toll-like receptors ; Tumor necrosis factor- alpha</subject><ispartof>Journal of neurochemistry, 2012-03, Vol.120 (6), p.1060-1071</ispartof><rights>2012 The Authors. Journal of Neurochemistry © 2012 International Society for Neurochemistry</rights><rights>2015 INIST-CNRS</rights><rights>2012 The Authors. Journal of Neurochemistry © 2012 International Society for Neurochemistry.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6660-6107be982f8e9da86834cc8eda958640c10883119e19ac95675b52cc6bab6ed3</citedby><cites>FETCH-LOGICAL-c6660-6107be982f8e9da86834cc8eda958640c10883119e19ac95675b52cc6bab6ed3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1471-4159.2012.07660.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1471-4159.2012.07660.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,1427,27903,27904,45553,45554,46388,46812</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25603981$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22248073$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gupta, Sunita</creatorcontrib><creatorcontrib>Knight, Alecia G.</creatorcontrib><creatorcontrib>Gupta, Shruti</creatorcontrib><creatorcontrib>Keller, Jeffrey N.</creatorcontrib><creatorcontrib>Bruce-Keller, Annadora J.</creatorcontrib><title>Saturated long-chain fatty acids activate inflammatory signaling in astrocytes</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>J. Neurochem. (2012) 120, 1060–1071.
This study describes the effects of long‐chain fatty acids on inflammatory signaling in cultured astrocytes. Data show that the saturated fatty acid palmitic acid, as well as lauric acid and stearic acid, trigger the release of TNFα and IL‐6 from astrocytes. Unsaturated fatty acids were unable to induce cytokine release from cultured astrocytes. Furthermore, the effects of palmitic acid on cytokine release require Toll‐like receptor 4 rather than CD36 or Toll‐like receptor 2, and do not depend on palmitic acid metabolism to palmitoyl‐CoA. Inhibitor studies revealed that pharmacologic inhibition of p38 or p42/44 MAPK pathways prevents the pro‐inflammatory effects of palmitic acid, whereas JNK and PI3K inhibition does not affect cytokine release. Depletion of microglia from primary astrocyte cultures using the lysosomotropic agent l‐leucine methyl ester revealed that the ability of palmitic acid to trigger cytokine release is not dependent on the presence of microglia. Finally, data show that the essential ω‐3 fatty acid docosahexaenoic acid acts in a dose‐dependent manner to prevent the actions of palmitic acid on inflammatory signaling in astrocytes. Collectively, these data demonstrate the ability of saturated fatty acids to induce astrocyte inflammation in vitro. These data thus raise the possibility that high levels of circulating saturated fatty acids could cause reactive gliosis and brain inflammation in vivo, and could potentially participate in the reported adverse neurologic consequences of obesity and metabolic syndrome.
The good fat, the bad fat, and the brain
Obesity and metabolic syndrome detrimentally affect the brain through unknown mechanisms. This paper demonstrates the ability of saturated fatty acids to trigger cytokine release from cultured astrocytes, and the ability of ω‐3 unsaturated fatty acids to block cytokine release. These data suggest that circulating saturated fatty acids could cause brain inflammation and thus participate in the adverse neurologic consequences of metabolic syndrome</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Astrocytes</subject><subject>Astrocytes - drug effects</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Brain - cytology</subject><subject>brain inflammation</subject><subject>c-Jun amino-terminal kinase</subject><subject>CD36 antigen</subject><subject>Cells</subject><subject>Cells, Cultured</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Data processing</subject><subject>Docosahexaenoic acid</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Interactions</subject><subject>dyslipidemia</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Fatty acids</subject><subject>Fatty Acids - metabolism</subject><subject>Fatty Acids - pharmacology</subject><subject>Female</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gliosis</subject><subject>Inflammation</subject><subject>Male</subject><subject>MAP kinase</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Metabolic disorders</subject><subject>Microglia</subject><subject>Miscellaneous</subject><subject>Neurochemistry</subject><subject>Obesity</subject><subject>Oleic Acid - pharmacology</subject><subject>Other metabolic disorders</subject><subject>Palmitic acid</subject><subject>Palmitic Acid - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>reactive gliosis</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Stearic acid</subject><subject>Toll-Like Receptor 2 - metabolism</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>Toll-like receptors</subject><subject>Tumor necrosis factor- alpha</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkVtv1DAQhS0EotvCX0AREuIpwZfYcR5AqlZQLmWRYKVKvFgTx9l6yaXYTrv59zjsslye8IM98nznaEYHoYTgjMTzYpuRvCBpTniZUUxohgshcLa7hxbHxn20wJjSlOGcnqBT77cYE5EL8hCdUEpziQu2QKsvEEYHwdRJO_SbVF-D7ZMGQpgS0Lb28Q72NgKJ7ZsWug7C4KbE200Pre038TsBH9ygp2D8I_Sggdabx4f3DK3fvF4v36aXny7eLc8vUy3ioKkguKhMKWkjTVmDFJLlWktTQ8mlyLEmWEpGSGlICbrkouAVp1qLCiphanaGXu1tb8aqM7U2fXDQqhtnO3CTGsCqvzu9vVab4VYxWgpJcTR4fjBww_fR-KA667VpW-jNMHoVKVIwyopIPv2H3A6ji7tHiArOacFnSO4h7QbvnWmOoxCs5sTUVs3BqDkYNSemfiamdlH65M9VjsJfEUXg2QEAr6FtHPTa-t8cF5iVkkTu5Z67s62Z_nsA9X61nKuoT_d664PZHfXgvilRsIKrq9WFwuurz1_lh6X6yH4ANX3B2A</recordid><startdate>201203</startdate><enddate>201203</enddate><creator>Gupta, Sunita</creator><creator>Knight, Alecia G.</creator><creator>Gupta, Shruti</creator><creator>Keller, Jeffrey N.</creator><creator>Bruce-Keller, Annadora J.</creator><general>Blackwell Publishing Ltd</general><general>Wiley-Blackwell</general><scope>BSCLL</scope><scope>IQODW</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>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>5PM</scope></search><sort><creationdate>201203</creationdate><title>Saturated long-chain fatty acids activate inflammatory signaling in astrocytes</title><author>Gupta, Sunita ; Knight, Alecia G. ; Gupta, Shruti ; Keller, Jeffrey N. ; Bruce-Keller, Annadora J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6660-6107be982f8e9da86834cc8eda958640c10883119e19ac95675b52cc6bab6ed3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Astrocytes</topic><topic>Astrocytes - drug effects</topic><topic>Biological and medical sciences</topic><topic>Brain</topic><topic>Brain - cytology</topic><topic>brain inflammation</topic><topic>c-Jun amino-terminal kinase</topic><topic>CD36 antigen</topic><topic>Cells</topic><topic>Cells, Cultured</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Data processing</topic><topic>Docosahexaenoic acid</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Interactions</topic><topic>dyslipidemia</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Fatty acids</topic><topic>Fatty Acids - metabolism</topic><topic>Fatty Acids - pharmacology</topic><topic>Female</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gliosis</topic><topic>Inflammation</topic><topic>Male</topic><topic>MAP kinase</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Metabolic disorders</topic><topic>Microglia</topic><topic>Miscellaneous</topic><topic>Neurochemistry</topic><topic>Obesity</topic><topic>Oleic Acid - pharmacology</topic><topic>Other metabolic disorders</topic><topic>Palmitic acid</topic><topic>Palmitic Acid - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>reactive gliosis</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Stearic acid</topic><topic>Toll-Like Receptor 2 - metabolism</topic><topic>Toll-Like Receptor 4 - metabolism</topic><topic>Toll-like receptors</topic><topic>Tumor necrosis factor- alpha</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gupta, Sunita</creatorcontrib><creatorcontrib>Knight, Alecia G.</creatorcontrib><creatorcontrib>Gupta, Shruti</creatorcontrib><creatorcontrib>Keller, Jeffrey N.</creatorcontrib><creatorcontrib>Bruce-Keller, Annadora J.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gupta, Sunita</au><au>Knight, Alecia G.</au><au>Gupta, Shruti</au><au>Keller, Jeffrey N.</au><au>Bruce-Keller, Annadora J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Saturated long-chain fatty acids activate inflammatory signaling in astrocytes</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2012-03</date><risdate>2012</risdate><volume>120</volume><issue>6</issue><spage>1060</spage><epage>1071</epage><pages>1060-1071</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>J. Neurochem. (2012) 120, 1060–1071.
This study describes the effects of long‐chain fatty acids on inflammatory signaling in cultured astrocytes. Data show that the saturated fatty acid palmitic acid, as well as lauric acid and stearic acid, trigger the release of TNFα and IL‐6 from astrocytes. Unsaturated fatty acids were unable to induce cytokine release from cultured astrocytes. Furthermore, the effects of palmitic acid on cytokine release require Toll‐like receptor 4 rather than CD36 or Toll‐like receptor 2, and do not depend on palmitic acid metabolism to palmitoyl‐CoA. Inhibitor studies revealed that pharmacologic inhibition of p38 or p42/44 MAPK pathways prevents the pro‐inflammatory effects of palmitic acid, whereas JNK and PI3K inhibition does not affect cytokine release. Depletion of microglia from primary astrocyte cultures using the lysosomotropic agent l‐leucine methyl ester revealed that the ability of palmitic acid to trigger cytokine release is not dependent on the presence of microglia. Finally, data show that the essential ω‐3 fatty acid docosahexaenoic acid acts in a dose‐dependent manner to prevent the actions of palmitic acid on inflammatory signaling in astrocytes. Collectively, these data demonstrate the ability of saturated fatty acids to induce astrocyte inflammation in vitro. These data thus raise the possibility that high levels of circulating saturated fatty acids could cause reactive gliosis and brain inflammation in vivo, and could potentially participate in the reported adverse neurologic consequences of obesity and metabolic syndrome.
The good fat, the bad fat, and the brain
Obesity and metabolic syndrome detrimentally affect the brain through unknown mechanisms. This paper demonstrates the ability of saturated fatty acids to trigger cytokine release from cultured astrocytes, and the ability of ω‐3 unsaturated fatty acids to block cytokine release. These data suggest that circulating saturated fatty acids could cause brain inflammation and thus participate in the adverse neurologic consequences of metabolic syndrome</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>22248073</pmid><doi>10.1111/j.1471-4159.2012.07660.x</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Animals, Newborn Astrocytes Astrocytes - drug effects Biological and medical sciences Brain Brain - cytology brain inflammation c-Jun amino-terminal kinase CD36 antigen Cells Cells, Cultured Cytokines Cytokines - metabolism Data processing Docosahexaenoic acid Dose-Response Relationship, Drug Drug Interactions dyslipidemia Enzyme Inhibitors - pharmacology Enzyme-Linked Immunosorbent Assay Fatty acids Fatty Acids - metabolism Fatty Acids - pharmacology Female Gene Expression Regulation - drug effects Gliosis Inflammation Male MAP kinase Medical sciences Metabolic diseases Metabolic disorders Microglia Miscellaneous Neurochemistry Obesity Oleic Acid - pharmacology Other metabolic disorders Palmitic acid Palmitic Acid - pharmacology Rats Rats, Sprague-Dawley reactive gliosis Signal transduction Signal Transduction - drug effects Stearic acid Toll-Like Receptor 2 - metabolism Toll-Like Receptor 4 - metabolism Toll-like receptors Tumor necrosis factor- alpha |
| title | Saturated long-chain fatty acids activate inflammatory signaling in astrocytes |
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