Effect of pitavastatin on experimental choroidal neovascularization in rats
The association between the use of statins and age-related macular degeneration (AMD), a leading cause of blindness, has been evaluated in many clinical studies; however, the results have been contradictory. We evaluated the effect of pitavastatin administration on laser-induced experimental choroid...
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Veröffentlicht in: | Experimental eye research 2007-06, Vol.84 (6), p.1074-1080 |
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description | The association between the use of statins and age-related macular degeneration (AMD), a leading cause of blindness, has been evaluated in many clinical studies; however, the results have been contradictory. We evaluated the effect of pitavastatin administration on laser-induced experimental choroidal neovascularization (CNV) in rats. Brown Norway rats received pitavastatin (1.0
mg/kg per day) for 1
day prior to laser-induced CNV and continued to receive the drug for 14
days. Fluorescein angiograms were graded by masked observers. CNV area and thickness were assessed by fluorescein isothiocyanate-labeled dextran angiography and histology, respectively. Vascular endothelial growth factor (VEGF), monocyte chemoattractant protein-1 (Ccl-2; also known as MCP-1), and intercellular adhesion molecule-1 (ICAM-1) mRNA levels were measured using reverse-transcription polymerase chain reaction (RT-PCR) and real-time quantitative RT-PCR. Pitavastatin-treated rats had significantly less fluorescence leakage compared with the vehicle-treated rats estimated by CNV score using fluorescein angiography. Both the area and the thickness of CNV in pitavastatin-treated rats were significantly reduced compared with the vehicle-treated rats. Gene expression of VEGF, Ccl-2, and ICAM-1 were significantly decreased by pitavastatin administration in experimental CNV. Thus, we demonstrated that the therapeutic dose of pitavastatin for human hypocholesterolemia effectively suppressed experimental CNV in rats. The use of pitavastatin may be helpful in preventing CNV development in AMD patients. |
doi_str_mv | 10.1016/j.exer.2007.02.005 |
format | Article |
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mg/kg per day) for 1
day prior to laser-induced CNV and continued to receive the drug for 14
days. Fluorescein angiograms were graded by masked observers. CNV area and thickness were assessed by fluorescein isothiocyanate-labeled dextran angiography and histology, respectively. Vascular endothelial growth factor (VEGF), monocyte chemoattractant protein-1 (Ccl-2; also known as MCP-1), and intercellular adhesion molecule-1 (ICAM-1) mRNA levels were measured using reverse-transcription polymerase chain reaction (RT-PCR) and real-time quantitative RT-PCR. Pitavastatin-treated rats had significantly less fluorescence leakage compared with the vehicle-treated rats estimated by CNV score using fluorescein angiography. Both the area and the thickness of CNV in pitavastatin-treated rats were significantly reduced compared with the vehicle-treated rats. Gene expression of VEGF, Ccl-2, and ICAM-1 were significantly decreased by pitavastatin administration in experimental CNV. Thus, we demonstrated that the therapeutic dose of pitavastatin for human hypocholesterolemia effectively suppressed experimental CNV in rats. The use of pitavastatin may be helpful in preventing CNV development in AMD patients.</description><identifier>ISSN: 0014-4835</identifier><identifier>EISSN: 1096-0007</identifier><identifier>DOI: 10.1016/j.exer.2007.02.005</identifier><identifier>PMID: 17418120</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>age-related macular degeneration ; Animals ; Chemokine CCL2 - biosynthesis ; Chemokine CCL2 - genetics ; choroidal neovascularization ; Choroidal Neovascularization - metabolism ; Choroidal Neovascularization - pathology ; Choroidal Neovascularization - prevention & control ; Drug Evaluation, Preclinical ; Fluorescein Angiography ; Gene Expression Regulation - drug effects ; HMG-CoA reductase inhibitor ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use ; Intercellular Adhesion Molecule-1 - biosynthesis ; Intercellular Adhesion Molecule-1 - genetics ; Male ; pitavastatin ; Quinolines - therapeutic use ; Rats ; Rats, Inbred BN ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - genetics ; Severity of Illness Index ; Vascular Endothelial Growth Factor A - biosynthesis ; Vascular Endothelial Growth Factor A - genetics</subject><ispartof>Experimental eye research, 2007-06, Vol.84 (6), p.1074-1080</ispartof><rights>2007 Elsevier Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c354t-184dac8bea57a3963a8d640eac927aeff00c8603d6ac5c5bc91355ba548929073</citedby><cites>FETCH-LOGICAL-c354t-184dac8bea57a3963a8d640eac927aeff00c8603d6ac5c5bc91355ba548929073</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.exer.2007.02.005$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27907,27908,45978</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17418120$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sagara, Nina</creatorcontrib><creatorcontrib>Kawaji, Takahiro</creatorcontrib><creatorcontrib>Takano, Akiomi</creatorcontrib><creatorcontrib>Inomata, Yasuya</creatorcontrib><creatorcontrib>Inatani, Masaru</creatorcontrib><creatorcontrib>Fukushima, Mikiko</creatorcontrib><creatorcontrib>Tanihara, Hidenobu</creatorcontrib><title>Effect of pitavastatin on experimental choroidal neovascularization in rats</title><title>Experimental eye research</title><addtitle>Exp Eye Res</addtitle><description>The association between the use of statins and age-related macular degeneration (AMD), a leading cause of blindness, has been evaluated in many clinical studies; however, the results have been contradictory. We evaluated the effect of pitavastatin administration on laser-induced experimental choroidal neovascularization (CNV) in rats. Brown Norway rats received pitavastatin (1.0
mg/kg per day) for 1
day prior to laser-induced CNV and continued to receive the drug for 14
days. Fluorescein angiograms were graded by masked observers. CNV area and thickness were assessed by fluorescein isothiocyanate-labeled dextran angiography and histology, respectively. Vascular endothelial growth factor (VEGF), monocyte chemoattractant protein-1 (Ccl-2; also known as MCP-1), and intercellular adhesion molecule-1 (ICAM-1) mRNA levels were measured using reverse-transcription polymerase chain reaction (RT-PCR) and real-time quantitative RT-PCR. Pitavastatin-treated rats had significantly less fluorescence leakage compared with the vehicle-treated rats estimated by CNV score using fluorescein angiography. Both the area and the thickness of CNV in pitavastatin-treated rats were significantly reduced compared with the vehicle-treated rats. Gene expression of VEGF, Ccl-2, and ICAM-1 were significantly decreased by pitavastatin administration in experimental CNV. Thus, we demonstrated that the therapeutic dose of pitavastatin for human hypocholesterolemia effectively suppressed experimental CNV in rats. The use of pitavastatin may be helpful in preventing CNV development in AMD patients.</description><subject>age-related macular degeneration</subject><subject>Animals</subject><subject>Chemokine CCL2 - biosynthesis</subject><subject>Chemokine CCL2 - genetics</subject><subject>choroidal neovascularization</subject><subject>Choroidal Neovascularization - metabolism</subject><subject>Choroidal Neovascularization - pathology</subject><subject>Choroidal Neovascularization - prevention & control</subject><subject>Drug Evaluation, Preclinical</subject><subject>Fluorescein Angiography</subject><subject>Gene Expression Regulation - drug effects</subject><subject>HMG-CoA reductase inhibitor</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</subject><subject>Intercellular Adhesion Molecule-1 - biosynthesis</subject><subject>Intercellular Adhesion Molecule-1 - genetics</subject><subject>Male</subject><subject>pitavastatin</subject><subject>Quinolines - therapeutic use</subject><subject>Rats</subject><subject>Rats, Inbred BN</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - genetics</subject><subject>Severity of Illness Index</subject><subject>Vascular Endothelial Growth Factor A - biosynthesis</subject><subject>Vascular Endothelial Growth Factor A - genetics</subject><issn>0014-4835</issn><issn>1096-0007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kD1PwzAQhi0EoqXwBxhQJraEc2zHicSCqvIhKrHAbF2di3CVJsVOq8Kvx1UrsTH5dHreV76HsWsOGQde3C0z2pHPcgCdQZ4BqBM25lAVKcTVKRsDcJnKUqgRuwhhGbdCannORlxLXvIcxux11jRkh6RvkrUbcIthwMF1Sd8ltFuTdyvqBmwT-9n73tVx6qiPlN206N1PZCMZeY9DuGRnDbaBro7vhH08zt6nz-n87ell-jBPrVBySHkpa7TlglBpFFUhsKwLCYS2yjVS0wDYsgBRF2iVVQtbcaHUApUsq7wCLSbs9tC79v3XhsJgVi5YaluMf9sEo0EVWugigvkBtL4PwVNj1vEg9N-Gg9krNEuzV2j2Cg3kJiqMoZtj-2axovovcnQWgfsDQPHGrYvxYB11lmrno0pT9-6__l_lnYN3</recordid><startdate>20070601</startdate><enddate>20070601</enddate><creator>Sagara, Nina</creator><creator>Kawaji, Takahiro</creator><creator>Takano, Akiomi</creator><creator>Inomata, Yasuya</creator><creator>Inatani, Masaru</creator><creator>Fukushima, Mikiko</creator><creator>Tanihara, Hidenobu</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>7X8</scope></search><sort><creationdate>20070601</creationdate><title>Effect of pitavastatin on experimental choroidal neovascularization in rats</title><author>Sagara, Nina ; Kawaji, Takahiro ; Takano, Akiomi ; Inomata, Yasuya ; Inatani, Masaru ; Fukushima, Mikiko ; Tanihara, Hidenobu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c354t-184dac8bea57a3963a8d640eac927aeff00c8603d6ac5c5bc91355ba548929073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>age-related macular degeneration</topic><topic>Animals</topic><topic>Chemokine CCL2 - biosynthesis</topic><topic>Chemokine CCL2 - genetics</topic><topic>choroidal neovascularization</topic><topic>Choroidal Neovascularization - metabolism</topic><topic>Choroidal Neovascularization - pathology</topic><topic>Choroidal Neovascularization - prevention & control</topic><topic>Drug Evaluation, Preclinical</topic><topic>Fluorescein Angiography</topic><topic>Gene Expression Regulation - drug effects</topic><topic>HMG-CoA reductase inhibitor</topic><topic>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</topic><topic>Intercellular Adhesion Molecule-1 - biosynthesis</topic><topic>Intercellular Adhesion Molecule-1 - genetics</topic><topic>Male</topic><topic>pitavastatin</topic><topic>Quinolines - therapeutic use</topic><topic>Rats</topic><topic>Rats, Inbred BN</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - methods</topic><topic>RNA, Messenger - genetics</topic><topic>Severity of Illness Index</topic><topic>Vascular Endothelial Growth Factor A - biosynthesis</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sagara, Nina</creatorcontrib><creatorcontrib>Kawaji, Takahiro</creatorcontrib><creatorcontrib>Takano, Akiomi</creatorcontrib><creatorcontrib>Inomata, Yasuya</creatorcontrib><creatorcontrib>Inatani, Masaru</creatorcontrib><creatorcontrib>Fukushima, Mikiko</creatorcontrib><creatorcontrib>Tanihara, Hidenobu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental eye research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sagara, Nina</au><au>Kawaji, Takahiro</au><au>Takano, Akiomi</au><au>Inomata, Yasuya</au><au>Inatani, Masaru</au><au>Fukushima, Mikiko</au><au>Tanihara, Hidenobu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of pitavastatin on experimental choroidal neovascularization in rats</atitle><jtitle>Experimental eye research</jtitle><addtitle>Exp Eye Res</addtitle><date>2007-06-01</date><risdate>2007</risdate><volume>84</volume><issue>6</issue><spage>1074</spage><epage>1080</epage><pages>1074-1080</pages><issn>0014-4835</issn><eissn>1096-0007</eissn><abstract>The association between the use of statins and age-related macular degeneration (AMD), a leading cause of blindness, has been evaluated in many clinical studies; however, the results have been contradictory. We evaluated the effect of pitavastatin administration on laser-induced experimental choroidal neovascularization (CNV) in rats. Brown Norway rats received pitavastatin (1.0
mg/kg per day) for 1
day prior to laser-induced CNV and continued to receive the drug for 14
days. Fluorescein angiograms were graded by masked observers. CNV area and thickness were assessed by fluorescein isothiocyanate-labeled dextran angiography and histology, respectively. Vascular endothelial growth factor (VEGF), monocyte chemoattractant protein-1 (Ccl-2; also known as MCP-1), and intercellular adhesion molecule-1 (ICAM-1) mRNA levels were measured using reverse-transcription polymerase chain reaction (RT-PCR) and real-time quantitative RT-PCR. Pitavastatin-treated rats had significantly less fluorescence leakage compared with the vehicle-treated rats estimated by CNV score using fluorescein angiography. Both the area and the thickness of CNV in pitavastatin-treated rats were significantly reduced compared with the vehicle-treated rats. Gene expression of VEGF, Ccl-2, and ICAM-1 were significantly decreased by pitavastatin administration in experimental CNV. Thus, we demonstrated that the therapeutic dose of pitavastatin for human hypocholesterolemia effectively suppressed experimental CNV in rats. The use of pitavastatin may be helpful in preventing CNV development in AMD patients.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>17418120</pmid><doi>10.1016/j.exer.2007.02.005</doi><tpages>7</tpages></addata></record> |
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subjects | age-related macular degeneration Animals Chemokine CCL2 - biosynthesis Chemokine CCL2 - genetics choroidal neovascularization Choroidal Neovascularization - metabolism Choroidal Neovascularization - pathology Choroidal Neovascularization - prevention & control Drug Evaluation, Preclinical Fluorescein Angiography Gene Expression Regulation - drug effects HMG-CoA reductase inhibitor Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use Intercellular Adhesion Molecule-1 - biosynthesis Intercellular Adhesion Molecule-1 - genetics Male pitavastatin Quinolines - therapeutic use Rats Rats, Inbred BN Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - genetics Severity of Illness Index Vascular Endothelial Growth Factor A - biosynthesis Vascular Endothelial Growth Factor A - genetics |
title | Effect of pitavastatin on experimental choroidal neovascularization in rats |
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