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
Hauptverfasser: Sagara, Nina, Kawaji, Takahiro, Takano, Akiomi, Inomata, Yasuya, Inatani, Masaru, Fukushima, Mikiko, Tanihara, Hidenobu
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container_end_page 1080
container_issue 6
container_start_page 1074
container_title Experimental eye research
container_volume 84
creator Sagara, Nina
Kawaji, Takahiro
Takano, Akiomi
Inomata, Yasuya
Inatani, Masaru
Fukushima, Mikiko
Tanihara, Hidenobu
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
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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. 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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 &amp; 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 ; 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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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source MEDLINE; ScienceDirect Journals (5 years ago - present)
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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