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Anti-Inflammatory Mechanism By Oxysterols In Cultured Rat Brain Astrocytes

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dc.contributor.author이, 창석-
dc.date.accessioned2011-01-31T05:54:37Z-
dc.date.available2011-01-31T05:54:37Z-
dc.date.issued2006-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/1388-
dc.description.abstract"Cholesterols are enriched in the brain and can be oxidized to oxysterols by spontaneous or enzyme-mediated processes. Oxysterols are transport forms of cholesterols across cell membranes and the blood-brain barrier. Here, to elucidate the roles of oxysterols in brain inflammation, I treated lipopolysaccharides(LPS)- or interferon gamma(IFN-stimulated rat brain astrocytes with two oxysterols, 7-ketocholesterol and 22(R)-hydroxycholesterol. In LPS-stimulated astrocytes, both oxysterols suppressed inducible nitric oxide synthase expression and nitric oxide release as well as upstream signaling molecules including interferon-, phosphorylated signal transducer and activator of transcription 1/3, and interferon regulatory factor-1. And oxysterols also inhibited interleukin-6 and tumor necrosis factor  transcripts, and monocyte chemoattractant protein-1 release. Oxysterols are known as nuclear receptor liver X receptor agonists, and these inhibitory effects were observed with synthetic agonists of liver X receptor and retinoid X receptor in a similar manner. In addition, ATP-binding cassette transporter a1 transcription, LXR-induced target gene, was increased by addition of either oxysterol or LXR agonist. Thus, I conclude that these effects are mediated by LXR/RXR heterodimers. Next, these inhibitory effects of oxysterols also appeared and were potentiated by RXR agonist in IFN-stimulated astrocytes. Furthermore, iNOS expression was inhibited by oxysterols and synthetic LXR ligands in LPS-stimulated primary microglia as well as in LPS- or IFN-stimulated primary astrocytes. I conclude that oxysterols suppress inflammatory gene expression through LXR/RXR activation in activated rat brain glial cells and these results provide new insights into the roles of oxysterols in brain inflammation."-
dc.description.tableofcontents"ABSTRACT ⅰ TABLE OF CONTENTS ⅲ LIST OF FIGURES ⅴ LIST OF TABLES ⅵ ABBREVIATION ⅶ I. INTRODUCTION 1 A. Cholesterol in brain 1 B. Oxysterol metabolism 3 C. LXRs in cholesterol metabolism and inflammation 5 D. Aims of study 7 II. MATERIALS AND METHODS 8 A. Reagents 8 B. Cell culture 8 C. Western Blot Analysis 9 D. Determination of NO release 9 E. Reverse transcription-polymerase chain reaction (RT-PCR) 10 F. Enzyme-linked immunosorbent assay (ELISA) 10 G. Data analysis 11 III. RESULTS 12 A. Oxysterols suppress iNOS, COX2 expression and NO production in LPS-stimulated rat brain astrocytes. 12 B. Suppression of iNOS expression by oxysterols occurs in a LXR/RXR heterodimer-dependent manner. 15 C. Oxysterols and synthetic LXR agonists suppress the expression of IFN- transcripts, phosphorylated STATs, and IRF-1 expression in LPS- stimulated primary astrocytes. 18 D. Oxysterols and synthetic LXR agonists suppress not only iNOS expression but the expression of IL-6 and TNFtranscripts, and MCP-1 release in LPS-stimulated primary astrocytes. 20 E. Oxysterols and synthetic LXR agonists suppress also iNOS expression in IFN-stimulated primary astrocytes and LPS-stimulated primary microglia 23 IV. DISCUSSION 27 V. CONCLUSION 29 REFERENCES 30 국문요약 39"-
dc.formattext/plain-
dc.language.isoen-
dc.titleAnti-Inflammatory Mechanism By Oxysterols In Cultured Rat Brain Astrocytes-
dc.title.alternative성상교세포에서 옥시스테롤의 항염증반응에 대한 연구-
dc.typeThesis-
dc.identifier.urlhttp://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000001229-
dc.subject.keywordoxysterols-
dc.subject.keywordLXR-
dc.subject.keywordiNOS-
dc.subject.keywordIFN-gamma-
dc.subject.keywordSTAT-
dc.subject.keywordIRF-1-
dc.subject.keywordastrocytes-
dc.description.degreeMaster-
dc.contributor.department대학원 의학과-
dc.contributor.affiliatedAuthor이, 창석-
dc.date.awarded2006-
dc.type.localTheses-
dc.citation.date2006-
dc.embargo.liftdate9999-12-31-
dc.embargo.terms9999-12-31-
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Theses > School of Medicine / Graduate School of Medicine > Master
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