Inhibition of choroidal neovascularization by homoisoflavanone, a new angiogenesis inhibitor
Age-related macular degeneration (AMD) is the leading cause of blindness in elderly. The detailed mechanism of choroidal neovascularization (CNV) leads to severe vision loss in patients with AMD. This study was undertaken to evaluate the inhibitory effect of homoisoflavanone on CNV. Antiangiogenic a...
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| Veröffentlicht in: | Molecular vision 2008-03, Vol.14, p.556-561 |
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| creator | Kim, Jeong Hun Kim, Jin Hyoung Yu, Young Suk Jun, Hyoung-Oh Kwon, Ho Jeong Park, Kyu Hyung Kim, Kyu-Won |
| description | Age-related macular degeneration (AMD) is the leading cause of blindness in elderly. The detailed mechanism of choroidal neovascularization (CNV) leads to severe vision loss in patients with AMD. This study was undertaken to evaluate the inhibitory effect of homoisoflavanone on CNV.
Antiangiogenic activity of homoisoflavanone was evaluated by in vitro tube formation assay of human umbilical vein endothelial cells (HUVECs) and cell migration assay of HUVECs., Homoisoflavanone or PBS was injected intravitreously into a mouse model of laser-photocoagulation-induced CNV. Fluorescein angiography and vessel counting in cross sections were employed to examine CNV lesions. The toxicity of homoisoflavanone was evaluated through 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (MTT) assay in HUVECs as well as histological examination and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining in the retina.
Homoisoflavanone effectively inhibited in vitro tube formation and cell migration of HUVECs. Interestingly, homoisoflavanone significantly reduced CNV and its leakage in a mouse model of laser-photocoagulation-induced CNV. In addition, homoisoflavanone showed no effect on cell viability of HUVECs and no retinal toxicity in a concentration range of 1-10 microM.
Our data suggest that homoisoflavanone is a potent inhibitor of CNV and may be applied in the treatment of other vasoproliferative retinopathies and tumor. |
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Antiangiogenic activity of homoisoflavanone was evaluated by in vitro tube formation assay of human umbilical vein endothelial cells (HUVECs) and cell migration assay of HUVECs., Homoisoflavanone or PBS was injected intravitreously into a mouse model of laser-photocoagulation-induced CNV. Fluorescein angiography and vessel counting in cross sections were employed to examine CNV lesions. The toxicity of homoisoflavanone was evaluated through 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (MTT) assay in HUVECs as well as histological examination and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining in the retina.
Homoisoflavanone effectively inhibited in vitro tube formation and cell migration of HUVECs. Interestingly, homoisoflavanone significantly reduced CNV and its leakage in a mouse model of laser-photocoagulation-induced CNV. In addition, homoisoflavanone showed no effect on cell viability of HUVECs and no retinal toxicity in a concentration range of 1-10 microM.
Our data suggest that homoisoflavanone is a potent inhibitor of CNV and may be applied in the treatment of other vasoproliferative retinopathies and tumor.</description><identifier>EISSN: 1090-0535</identifier><identifier>PMID: 18385791</identifier><language>eng</language><publisher>United States: Molecular Vision</publisher><subject>Angiogenesis Inhibitors - administration & dosage ; Angiogenesis Inhibitors - pharmacology ; Animals ; Capillary Permeability - drug effects ; Cell Movement - drug effects ; Cell Survival - drug effects ; Choroidal Neovascularization - etiology ; Choroidal Neovascularization - metabolism ; Choroidal Neovascularization - pathology ; Choroidal Neovascularization - prevention & control ; Dose-Response Relationship, Drug ; Endothelial Cells - drug effects ; Female ; Humans ; Isoflavones - administration & dosage ; Isoflavones - pharmacology ; Laser Coagulation ; Mice ; Mice, Inbred C57BL ; Retina - drug effects</subject><ispartof>Molecular vision, 2008-03, Vol.14, p.556-561</ispartof><rights>2008 Molecular Vision</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2274926/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2274926/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18385791$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Jeong Hun</creatorcontrib><creatorcontrib>Kim, Jin Hyoung</creatorcontrib><creatorcontrib>Yu, Young Suk</creatorcontrib><creatorcontrib>Jun, Hyoung-Oh</creatorcontrib><creatorcontrib>Kwon, Ho Jeong</creatorcontrib><creatorcontrib>Park, Kyu Hyung</creatorcontrib><creatorcontrib>Kim, Kyu-Won</creatorcontrib><title>Inhibition of choroidal neovascularization by homoisoflavanone, a new angiogenesis inhibitor</title><title>Molecular vision</title><addtitle>Mol Vis</addtitle><description>Age-related macular degeneration (AMD) is the leading cause of blindness in elderly. The detailed mechanism of choroidal neovascularization (CNV) leads to severe vision loss in patients with AMD. This study was undertaken to evaluate the inhibitory effect of homoisoflavanone on CNV.
Antiangiogenic activity of homoisoflavanone was evaluated by in vitro tube formation assay of human umbilical vein endothelial cells (HUVECs) and cell migration assay of HUVECs., Homoisoflavanone or PBS was injected intravitreously into a mouse model of laser-photocoagulation-induced CNV. Fluorescein angiography and vessel counting in cross sections were employed to examine CNV lesions. The toxicity of homoisoflavanone was evaluated through 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (MTT) assay in HUVECs as well as histological examination and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining in the retina.
Homoisoflavanone effectively inhibited in vitro tube formation and cell migration of HUVECs. Interestingly, homoisoflavanone significantly reduced CNV and its leakage in a mouse model of laser-photocoagulation-induced CNV. In addition, homoisoflavanone showed no effect on cell viability of HUVECs and no retinal toxicity in a concentration range of 1-10 microM.
Our data suggest that homoisoflavanone is a potent inhibitor of CNV and may be applied in the treatment of other vasoproliferative retinopathies and tumor.</description><subject>Angiogenesis Inhibitors - administration & dosage</subject><subject>Angiogenesis Inhibitors - pharmacology</subject><subject>Animals</subject><subject>Capillary Permeability - drug effects</subject><subject>Cell Movement - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Choroidal Neovascularization - etiology</subject><subject>Choroidal Neovascularization - metabolism</subject><subject>Choroidal Neovascularization - pathology</subject><subject>Choroidal Neovascularization - prevention & control</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelial Cells - drug effects</subject><subject>Female</subject><subject>Humans</subject><subject>Isoflavones - administration & dosage</subject><subject>Isoflavones - pharmacology</subject><subject>Laser Coagulation</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Retina - drug effects</subject><issn>1090-0535</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkMtKAzEYhYMgtlZfQfIADuQ2M8lGkOKlUHCjO2H4k_zTiUyTMmlH6tNbrIquzuI751ucEzLlzLCClbKckPOc3xgTvFT1GZlwLXVZGz4lr4vYBRu2IUWaWuq6NKTgoacR0wjZ7XoYwgd8cbunXVqnkFPbwwgxRbymcGi-U4irkFYYMYdMw1GZhgty2kKf8fI7Z-Tl_u55_lgsnx4W89tlsRGV2hbgdGuUZ85WtZJtJWuNViJKrXSLnEkNtbdcWKacd9qw0qHhXpXMG6E0yhm5OXo3O7tG7zBuB-ibzRDWMOybBKH5T2LomlUaGyFqZUR1EFz9Ffwuf36Sn7GUZ2A</recordid><startdate>20080318</startdate><enddate>20080318</enddate><creator>Kim, Jeong Hun</creator><creator>Kim, Jin Hyoung</creator><creator>Yu, Young Suk</creator><creator>Jun, Hyoung-Oh</creator><creator>Kwon, Ho Jeong</creator><creator>Park, Kyu Hyung</creator><creator>Kim, Kyu-Won</creator><general>Molecular Vision</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>5PM</scope></search><sort><creationdate>20080318</creationdate><title>Inhibition of choroidal neovascularization by homoisoflavanone, a new angiogenesis inhibitor</title><author>Kim, Jeong Hun ; Kim, Jin Hyoung ; Yu, Young Suk ; Jun, Hyoung-Oh ; Kwon, Ho Jeong ; Park, Kyu Hyung ; Kim, Kyu-Won</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p264t-ac8f94d0cb6743f6378eb3ee3848fe1038a7db12b04cdc8905ce91d450d9248e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Angiogenesis Inhibitors - administration & dosage</topic><topic>Angiogenesis Inhibitors - pharmacology</topic><topic>Animals</topic><topic>Capillary Permeability - drug effects</topic><topic>Cell Movement - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Choroidal Neovascularization - etiology</topic><topic>Choroidal Neovascularization - metabolism</topic><topic>Choroidal Neovascularization - pathology</topic><topic>Choroidal Neovascularization - prevention & control</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endothelial Cells - drug effects</topic><topic>Female</topic><topic>Humans</topic><topic>Isoflavones - administration & dosage</topic><topic>Isoflavones - pharmacology</topic><topic>Laser Coagulation</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Retina - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Jeong Hun</creatorcontrib><creatorcontrib>Kim, Jin Hyoung</creatorcontrib><creatorcontrib>Yu, Young Suk</creatorcontrib><creatorcontrib>Jun, Hyoung-Oh</creatorcontrib><creatorcontrib>Kwon, Ho Jeong</creatorcontrib><creatorcontrib>Park, Kyu Hyung</creatorcontrib><creatorcontrib>Kim, Kyu-Won</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular vision</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Jeong Hun</au><au>Kim, Jin Hyoung</au><au>Yu, Young Suk</au><au>Jun, Hyoung-Oh</au><au>Kwon, Ho Jeong</au><au>Park, Kyu Hyung</au><au>Kim, Kyu-Won</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of choroidal neovascularization by homoisoflavanone, a new angiogenesis inhibitor</atitle><jtitle>Molecular vision</jtitle><addtitle>Mol Vis</addtitle><date>2008-03-18</date><risdate>2008</risdate><volume>14</volume><spage>556</spage><epage>561</epage><pages>556-561</pages><eissn>1090-0535</eissn><abstract>Age-related macular degeneration (AMD) is the leading cause of blindness in elderly. The detailed mechanism of choroidal neovascularization (CNV) leads to severe vision loss in patients with AMD. This study was undertaken to evaluate the inhibitory effect of homoisoflavanone on CNV.
Antiangiogenic activity of homoisoflavanone was evaluated by in vitro tube formation assay of human umbilical vein endothelial cells (HUVECs) and cell migration assay of HUVECs., Homoisoflavanone or PBS was injected intravitreously into a mouse model of laser-photocoagulation-induced CNV. Fluorescein angiography and vessel counting in cross sections were employed to examine CNV lesions. The toxicity of homoisoflavanone was evaluated through 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (MTT) assay in HUVECs as well as histological examination and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining in the retina.
Homoisoflavanone effectively inhibited in vitro tube formation and cell migration of HUVECs. Interestingly, homoisoflavanone significantly reduced CNV and its leakage in a mouse model of laser-photocoagulation-induced CNV. In addition, homoisoflavanone showed no effect on cell viability of HUVECs and no retinal toxicity in a concentration range of 1-10 microM.
Our data suggest that homoisoflavanone is a potent inhibitor of CNV and may be applied in the treatment of other vasoproliferative retinopathies and tumor.</abstract><cop>United States</cop><pub>Molecular Vision</pub><pmid>18385791</pmid><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiogenesis Inhibitors - administration & dosage Angiogenesis Inhibitors - pharmacology Animals Capillary Permeability - drug effects Cell Movement - drug effects Cell Survival - drug effects Choroidal Neovascularization - etiology Choroidal Neovascularization - metabolism Choroidal Neovascularization - pathology Choroidal Neovascularization - prevention & control Dose-Response Relationship, Drug Endothelial Cells - drug effects Female Humans Isoflavones - administration & dosage Isoflavones - pharmacology Laser Coagulation Mice Mice, Inbred C57BL Retina - drug effects |
| title | Inhibition of choroidal neovascularization by homoisoflavanone, a new angiogenesis inhibitor |
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