Minocycline inhibits LPS-induced retinal microglia activation
Retinal neurodegenerative disease involves an inflammatory response in the retina characterized by an increase in inflammatory cytokines and activation of microglia. The degree of microglia activation may influence the extent of retinal injury following an inflammatory stimulus. Cytokines released b...
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| Veröffentlicht in: | Neurochemistry international 2005-07, Vol.47 (1), p.152-158 |
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| creator | Wang, Ai Ling Yu, Albert C.H. Lau, Lok Ting Lee, Chong Wu, Le Meng Zhu, Xiu’An Tso, Mark O.M. |
| description | Retinal neurodegenerative disease involves an inflammatory response in the retina characterized by an increase in inflammatory cytokines and activation of microglia. The degree of microglia activation may influence the extent of retinal injury following an inflammatory stimulus. Cytokines released by activated microglia regulate the influx of inflammatory cells to the damaged area. Thus, a therapeutic strategy to reduce cytokine expression in microglia would be neuroprotective. Minocycline, a semisynthetic tetracycline derivative, is known to protect rodent brain from ischemia and to inhibit microglial activation. In this study, we activated retinal microglia in culture with lipopolysaccharide (LPS) and attempted to determine whether minocycline could reduce the production of cytokines from activated microglia at both gene and protein levels. Changes in inflammatory cytokines, TNF-alpha and IL-1beta, were measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) in the presence or absence of LPS. We also measured the levels of nitric oxide (NO) by the nitrate reductase method under similar conditions. LPS treatment induced a significant upregulation of the mRNA and release of TNF-alpha, IL-1beta, and NO from retinal microglia. Minocycline inhibited these releases. Thus, minocycline might exert its antiinflammatory effect on microglia by inhibiting the expression and release of TNF-alpha, IL-1beta, and NO. |
| doi_str_mv | 10.1016/j.neuint.2005.04.018 |
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The degree of microglia activation may influence the extent of retinal injury following an inflammatory stimulus. Cytokines released by activated microglia regulate the influx of inflammatory cells to the damaged area. Thus, a therapeutic strategy to reduce cytokine expression in microglia would be neuroprotective. Minocycline, a semisynthetic tetracycline derivative, is known to protect rodent brain from ischemia and to inhibit microglial activation. In this study, we activated retinal microglia in culture with lipopolysaccharide (LPS) and attempted to determine whether minocycline could reduce the production of cytokines from activated microglia at both gene and protein levels. Changes in inflammatory cytokines, TNF-alpha and IL-1beta, were measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) in the presence or absence of LPS. We also measured the levels of nitric oxide (NO) by the nitrate reductase method under similar conditions. LPS treatment induced a significant upregulation of the mRNA and release of TNF-alpha, IL-1beta, and NO from retinal microglia. Minocycline inhibited these releases. Thus, minocycline might exert its antiinflammatory effect on microglia by inhibiting the expression and release of TNF-alpha, IL-1beta, and NO.</description><identifier>ISSN: 0197-0186</identifier><identifier>EISSN: 1872-9754</identifier><identifier>DOI: 10.1016/j.neuint.2005.04.018</identifier><identifier>PMID: 15904993</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Animals ; Animals, Newborn ; Anti-Bacterial Agents - pharmacology ; Anti-Inflammatory Agents - pharmacology ; Cells, Cultured ; Cytokines - antagonists & inhibitors ; Cytokines - genetics ; Cytokines - metabolism ; Diabetic Retinopathy - metabolism ; Diabetic Retinopathy - physiopathology ; Diabetic Retinopathy - prevention & control ; Encephalitis - chemically induced ; Encephalitis - drug therapy ; Encephalitis - physiopathology ; Gliosis - chemically induced ; Gliosis - physiopathology ; Gliosis - prevention & control ; IL-1beta ; Interleukin-1 - antagonists & inhibitors ; Interleukin-1 - genetics ; Interleukin-1 - metabolism ; Lipopolysaccharides ; LPS ; Microglia ; Microglia - drug effects ; Microglia - metabolism ; Minocycline ; Minocycline - pharmacology ; Minocycline - therapeutic use ; Neurodegenerative disease ; Neuroprotective Agents - pharmacology ; Nitric Oxide - metabolism ; Rats ; Rats, Sprague-Dawley ; Retina ; Retina - metabolism ; Retina - physiopathology ; TNF-alpha ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Up-Regulation - drug effects ; Up-Regulation - physiology</subject><ispartof>Neurochemistry international, 2005-07, Vol.47 (1), p.152-158</ispartof><rights>2005 Elsevier Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c457t-b0731b191380901533aac4689b25fc416dc844d7fb4a3457d9053ccc832f39943</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0197018605001038$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15904993$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Ai Ling</creatorcontrib><creatorcontrib>Yu, Albert C.H.</creatorcontrib><creatorcontrib>Lau, Lok Ting</creatorcontrib><creatorcontrib>Lee, Chong</creatorcontrib><creatorcontrib>Wu, Le Meng</creatorcontrib><creatorcontrib>Zhu, Xiu’An</creatorcontrib><creatorcontrib>Tso, Mark O.M.</creatorcontrib><title>Minocycline inhibits LPS-induced retinal microglia activation</title><title>Neurochemistry international</title><addtitle>Neurochem Int</addtitle><description>Retinal neurodegenerative disease involves an inflammatory response in the retina characterized by an increase in inflammatory cytokines and activation of microglia. The degree of microglia activation may influence the extent of retinal injury following an inflammatory stimulus. Cytokines released by activated microglia regulate the influx of inflammatory cells to the damaged area. Thus, a therapeutic strategy to reduce cytokine expression in microglia would be neuroprotective. Minocycline, a semisynthetic tetracycline derivative, is known to protect rodent brain from ischemia and to inhibit microglial activation. In this study, we activated retinal microglia in culture with lipopolysaccharide (LPS) and attempted to determine whether minocycline could reduce the production of cytokines from activated microglia at both gene and protein levels. Changes in inflammatory cytokines, TNF-alpha and IL-1beta, were measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) in the presence or absence of LPS. We also measured the levels of nitric oxide (NO) by the nitrate reductase method under similar conditions. LPS treatment induced a significant upregulation of the mRNA and release of TNF-alpha, IL-1beta, and NO from retinal microglia. Minocycline inhibited these releases. Thus, minocycline might exert its antiinflammatory effect on microglia by inhibiting the expression and release of TNF-alpha, IL-1beta, and NO.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Anti-Bacterial Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Cells, Cultured</subject><subject>Cytokines - antagonists & inhibitors</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Diabetic Retinopathy - metabolism</subject><subject>Diabetic Retinopathy - physiopathology</subject><subject>Diabetic Retinopathy - prevention & control</subject><subject>Encephalitis - chemically induced</subject><subject>Encephalitis - drug therapy</subject><subject>Encephalitis - physiopathology</subject><subject>Gliosis - chemically induced</subject><subject>Gliosis - physiopathology</subject><subject>Gliosis - prevention & control</subject><subject>IL-1beta</subject><subject>Interleukin-1 - antagonists & inhibitors</subject><subject>Interleukin-1 - genetics</subject><subject>Interleukin-1 - metabolism</subject><subject>Lipopolysaccharides</subject><subject>LPS</subject><subject>Microglia</subject><subject>Microglia - drug effects</subject><subject>Microglia - metabolism</subject><subject>Minocycline</subject><subject>Minocycline - pharmacology</subject><subject>Minocycline - therapeutic use</subject><subject>Neurodegenerative disease</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Nitric Oxide - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Retina</subject><subject>Retina - metabolism</subject><subject>Retina - physiopathology</subject><subject>TNF-alpha</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Up-Regulation - drug effects</subject><subject>Up-Regulation - physiology</subject><issn>0197-0186</issn><issn>1872-9754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE9LxDAQxYMo7rr6DUR68tY6adKmOSjI4j9YUVDPIU1TnaVNtWkX9tubpQvePA0M77158yPknEJCgeZX68TZEd2QpABZAjwBWhyQOS1EGkuR8UMyBypFHNb5jJx4vwYAISE7JjOaSeBSsjm5fkbXma1p0NkI3ReWOPho9foWo6tGY6uotwM63UQtmr77bFBH2gy40QN27pQc1brx9mw_F-Tj_u59-RivXh6elrer2PBMDHEJgtGSSsoKkEAzxrQ2PC9kmWa14TSvTMF5JeqSaxYcVWjJjDEFS2smJWcLcjnlfvfdz2j9oFr0xjaNdrYbvaKC5YKzNAj5JAxdve9trb57bHW_VRTUDptaqwmb2mFTwFXgE2wX-_yxbG31Z9pzCoKbSWDDlxu0vfIGrQt8sLdmUFWH_1_4BbWzf2g</recordid><startdate>20050701</startdate><enddate>20050701</enddate><creator>Wang, Ai Ling</creator><creator>Yu, Albert C.H.</creator><creator>Lau, Lok Ting</creator><creator>Lee, Chong</creator><creator>Wu, Le Meng</creator><creator>Zhu, Xiu’An</creator><creator>Tso, Mark O.M.</creator><general>Elsevier Ltd</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>7TK</scope></search><sort><creationdate>20050701</creationdate><title>Minocycline inhibits LPS-induced retinal microglia activation</title><author>Wang, Ai Ling ; Yu, Albert C.H. ; Lau, Lok Ting ; Lee, Chong ; Wu, Le Meng ; Zhu, Xiu’An ; Tso, Mark O.M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c457t-b0731b191380901533aac4689b25fc416dc844d7fb4a3457d9053ccc832f39943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Anti-Bacterial Agents - pharmacology</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Cells, Cultured</topic><topic>Cytokines - antagonists & inhibitors</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Diabetic Retinopathy - metabolism</topic><topic>Diabetic Retinopathy - physiopathology</topic><topic>Diabetic Retinopathy - prevention & control</topic><topic>Encephalitis - chemically induced</topic><topic>Encephalitis - drug therapy</topic><topic>Encephalitis - physiopathology</topic><topic>Gliosis - chemically induced</topic><topic>Gliosis - physiopathology</topic><topic>Gliosis - prevention & control</topic><topic>IL-1beta</topic><topic>Interleukin-1 - antagonists & inhibitors</topic><topic>Interleukin-1 - genetics</topic><topic>Interleukin-1 - metabolism</topic><topic>Lipopolysaccharides</topic><topic>LPS</topic><topic>Microglia</topic><topic>Microglia - drug effects</topic><topic>Microglia - metabolism</topic><topic>Minocycline</topic><topic>Minocycline - pharmacology</topic><topic>Minocycline - therapeutic use</topic><topic>Neurodegenerative disease</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Nitric Oxide - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Retina</topic><topic>Retina - metabolism</topic><topic>Retina - physiopathology</topic><topic>TNF-alpha</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Up-Regulation - drug effects</topic><topic>Up-Regulation - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Ai Ling</creatorcontrib><creatorcontrib>Yu, Albert C.H.</creatorcontrib><creatorcontrib>Lau, Lok Ting</creatorcontrib><creatorcontrib>Lee, Chong</creatorcontrib><creatorcontrib>Wu, Le Meng</creatorcontrib><creatorcontrib>Zhu, Xiu’An</creatorcontrib><creatorcontrib>Tso, Mark O.M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><jtitle>Neurochemistry international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Ai Ling</au><au>Yu, Albert C.H.</au><au>Lau, Lok Ting</au><au>Lee, Chong</au><au>Wu, Le Meng</au><au>Zhu, Xiu’An</au><au>Tso, Mark O.M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Minocycline inhibits LPS-induced retinal microglia activation</atitle><jtitle>Neurochemistry international</jtitle><addtitle>Neurochem Int</addtitle><date>2005-07-01</date><risdate>2005</risdate><volume>47</volume><issue>1</issue><spage>152</spage><epage>158</epage><pages>152-158</pages><issn>0197-0186</issn><eissn>1872-9754</eissn><abstract>Retinal neurodegenerative disease involves an inflammatory response in the retina characterized by an increase in inflammatory cytokines and activation of microglia. The degree of microglia activation may influence the extent of retinal injury following an inflammatory stimulus. Cytokines released by activated microglia regulate the influx of inflammatory cells to the damaged area. Thus, a therapeutic strategy to reduce cytokine expression in microglia would be neuroprotective. Minocycline, a semisynthetic tetracycline derivative, is known to protect rodent brain from ischemia and to inhibit microglial activation. In this study, we activated retinal microglia in culture with lipopolysaccharide (LPS) and attempted to determine whether minocycline could reduce the production of cytokines from activated microglia at both gene and protein levels. Changes in inflammatory cytokines, TNF-alpha and IL-1beta, were measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) in the presence or absence of LPS. We also measured the levels of nitric oxide (NO) by the nitrate reductase method under similar conditions. LPS treatment induced a significant upregulation of the mRNA and release of TNF-alpha, IL-1beta, and NO from retinal microglia. Minocycline inhibited these releases. Thus, minocycline might exert its antiinflammatory effect on microglia by inhibiting the expression and release of TNF-alpha, IL-1beta, and NO.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>15904993</pmid><doi>10.1016/j.neuint.2005.04.018</doi><tpages>7</tpages></addata></record> |
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| subjects | Animals Animals, Newborn Anti-Bacterial Agents - pharmacology Anti-Inflammatory Agents - pharmacology Cells, Cultured Cytokines - antagonists & inhibitors Cytokines - genetics Cytokines - metabolism Diabetic Retinopathy - metabolism Diabetic Retinopathy - physiopathology Diabetic Retinopathy - prevention & control Encephalitis - chemically induced Encephalitis - drug therapy Encephalitis - physiopathology Gliosis - chemically induced Gliosis - physiopathology Gliosis - prevention & control IL-1beta Interleukin-1 - antagonists & inhibitors Interleukin-1 - genetics Interleukin-1 - metabolism Lipopolysaccharides LPS Microglia Microglia - drug effects Microglia - metabolism Minocycline Minocycline - pharmacology Minocycline - therapeutic use Neurodegenerative disease Neuroprotective Agents - pharmacology Nitric Oxide - metabolism Rats Rats, Sprague-Dawley Retina Retina - metabolism Retina - physiopathology TNF-alpha Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Up-Regulation - drug effects Up-Regulation - physiology |
| title | Minocycline inhibits LPS-induced retinal microglia activation |
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