Effect of Lutein on Retinal Neurons and Oxidative Stress in a Model of Acute Retinal Ischemia/Reperfusion
Retinal ischemia/reperfusion (I/R) occurs in many ocular diseases and leads to neuronal death. Lutein, a potent antioxidant, is used to prevent severe visual loss in patients with early age-related macular degeneration (AMD), but its effect on I/R insult is unclear. The objective of the present stud...
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| Veröffentlicht in: | Investigative ophthalmology & visual science 2009-02, Vol.50 (2), p.836-843 |
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| creator | Li, Suk-Yee Fu, Zhong-Jie Ma, Huan Jang, Wai-Chi So, Kwok-Fai Wong, David Lo, Amy C. Y |
| description | Retinal ischemia/reperfusion (I/R) occurs in many ocular diseases and leads to neuronal death. Lutein, a potent antioxidant, is used to prevent severe visual loss in patients with early age-related macular degeneration (AMD), but its effect on I/R insult is unclear. The objective of the present study is to investigate the neuroprotective effect of lutein on retinal neurons after acute I/R injury.
Unilateral retinal I/R was induced by the blockade of internal carotid artery using intraluminal method in mice. Ischemia was maintained for 2 hours followed by 22 hours of reperfusion, during which either lutein or vehicle was administered. The number of viable retinal ganglion cells (RGC) was quantified. Apoptosis was investigated using TUNEL assay. Oxidative stress was elucidated using markers such as nitrotyrosine (NT) and poly(ADP-ribose) (PAR).
In vehicle-treated I/R retina, severe cell loss in ganglion cell layer, increased apoptosis as well as increased NT and nuclear PAR immunoreactivity were observed. In lutein-treated I/R retina, significantly less cell loss, decreased number of apoptotic cells, and decreased NT and nuclear PAR immunoreactivity were seen.
The neuroprotective effect of lutein was associated with reduced oxidative stress. Lutein has been hitherto used principally for protection of outer retinal elements in AMD. Our study suggests that it may also be relevant for the protection of inner retina from acute ischemic damage. |
| doi_str_mv | 10.1167/iovs.08-2310 |
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Unilateral retinal I/R was induced by the blockade of internal carotid artery using intraluminal method in mice. Ischemia was maintained for 2 hours followed by 22 hours of reperfusion, during which either lutein or vehicle was administered. The number of viable retinal ganglion cells (RGC) was quantified. Apoptosis was investigated using TUNEL assay. Oxidative stress was elucidated using markers such as nitrotyrosine (NT) and poly(ADP-ribose) (PAR).
In vehicle-treated I/R retina, severe cell loss in ganglion cell layer, increased apoptosis as well as increased NT and nuclear PAR immunoreactivity were observed. In lutein-treated I/R retina, significantly less cell loss, decreased number of apoptotic cells, and decreased NT and nuclear PAR immunoreactivity were seen.
The neuroprotective effect of lutein was associated with reduced oxidative stress. Lutein has been hitherto used principally for protection of outer retinal elements in AMD. Our study suggests that it may also be relevant for the protection of inner retina from acute ischemic damage.</description><identifier>ISSN: 0146-0404</identifier><identifier>ISSN: 1552-5783</identifier><identifier>EISSN: 1552-5783</identifier><identifier>DOI: 10.1167/iovs.08-2310</identifier><identifier>PMID: 18936152</identifier><identifier>CODEN: IOVSDA</identifier><language>eng</language><publisher>Rockville, MD: ARVO</publisher><subject>Acute Disease ; Animals ; Antioxidants - pharmacology ; Apoptosis ; Biological and medical sciences ; Calbindin 2 ; Cardiology. Vascular system ; Disease Models, Animal ; Eye and associated structures. Visual pathways and centers. Vision ; Fundamental and applied biological sciences. Psychology ; In Situ Nick-End Labeling ; Lutein - pharmacology ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Neurons - drug effects ; Neuroprotective Agents - pharmacology ; Ophthalmology ; Oxidative Stress - drug effects ; Poly Adenosine Diphosphate Ribose - metabolism ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Reperfusion Injury - prevention & control ; Retinal Diseases - metabolism ; Retinal Diseases - pathology ; Retinal Diseases - prevention & control ; Retinal Ganglion Cells - drug effects ; Retinal Ganglion Cells - pathology ; S100 Calcium Binding Protein G - metabolism ; Tyrosine - analogs & derivatives ; Tyrosine - metabolism ; Vertebrates: nervous system and sense organs</subject><ispartof>Investigative ophthalmology & visual science, 2009-02, Vol.50 (2), p.836-843</ispartof><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c453t-2f9d9292f430e91103754a5ef9ae15ae7c23760d266ae45aaf37a19d2d110b783</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21326271$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18936152$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Suk-Yee</creatorcontrib><creatorcontrib>Fu, Zhong-Jie</creatorcontrib><creatorcontrib>Ma, Huan</creatorcontrib><creatorcontrib>Jang, Wai-Chi</creatorcontrib><creatorcontrib>So, Kwok-Fai</creatorcontrib><creatorcontrib>Wong, David</creatorcontrib><creatorcontrib>Lo, Amy C. Y</creatorcontrib><title>Effect of Lutein on Retinal Neurons and Oxidative Stress in a Model of Acute Retinal Ischemia/Reperfusion</title><title>Investigative ophthalmology & visual science</title><addtitle>Invest Ophthalmol Vis Sci</addtitle><description>Retinal ischemia/reperfusion (I/R) occurs in many ocular diseases and leads to neuronal death. Lutein, a potent antioxidant, is used to prevent severe visual loss in patients with early age-related macular degeneration (AMD), but its effect on I/R insult is unclear. The objective of the present study is to investigate the neuroprotective effect of lutein on retinal neurons after acute I/R injury.
Unilateral retinal I/R was induced by the blockade of internal carotid artery using intraluminal method in mice. Ischemia was maintained for 2 hours followed by 22 hours of reperfusion, during which either lutein or vehicle was administered. The number of viable retinal ganglion cells (RGC) was quantified. Apoptosis was investigated using TUNEL assay. Oxidative stress was elucidated using markers such as nitrotyrosine (NT) and poly(ADP-ribose) (PAR).
In vehicle-treated I/R retina, severe cell loss in ganglion cell layer, increased apoptosis as well as increased NT and nuclear PAR immunoreactivity were observed. In lutein-treated I/R retina, significantly less cell loss, decreased number of apoptotic cells, and decreased NT and nuclear PAR immunoreactivity were seen.
The neuroprotective effect of lutein was associated with reduced oxidative stress. Lutein has been hitherto used principally for protection of outer retinal elements in AMD. Our study suggests that it may also be relevant for the protection of inner retina from acute ischemic damage.</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Calbindin 2</subject><subject>Cardiology. Vascular system</subject><subject>Disease Models, Animal</subject><subject>Eye and associated structures. Visual pathways and centers. Vision</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>In Situ Nick-End Labeling</subject><subject>Lutein - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Neurons - drug effects</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Ophthalmology</subject><subject>Oxidative Stress - drug effects</subject><subject>Poly Adenosine Diphosphate Ribose - metabolism</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Retinal Diseases - metabolism</subject><subject>Retinal Diseases - pathology</subject><subject>Retinal Diseases - prevention & control</subject><subject>Retinal Ganglion Cells - drug effects</subject><subject>Retinal Ganglion Cells - pathology</subject><subject>S100 Calcium Binding Protein G - metabolism</subject><subject>Tyrosine - analogs & derivatives</subject><subject>Tyrosine - metabolism</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0146-0404</issn><issn>1552-5783</issn><issn>1552-5783</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0EFP3DAQBWCragVb4NYz8qU9NeCxYyc5ohVtkbYg0fZsDc6YNUrixU5Y-u_JihWc5vK9J81j7AuIMwBTnYf4lM9EXUgF4gNbgNay0FWtPrKFgNIUohTlIfuc84MQEkCKA3YIdaMMaLlg4dJ7ciOPnq-mkcLA48BvaQwDdvyaphSHzHFo-c1zaHEMT8T_jIly5jNF_ju21O3CF25OvwWvsltTH_D8ljaU_JRDHI7ZJ49dppP9PWL_flz-Xf4qVjc_r5YXq8KVWo2F9E3byEb6UglqAISqdImafIMEGqlyUlVGtNIYpFIjelUhNK1sZ3s3_33Evr32blJ8nCiPtg_ZUdfhQHHK1phaK22aGX5_hS7FnBN5u0mhx_TfgrC7ae1uWitqu5t25qf73umup_Yd77ecwdc9wOyw8wkHF_Kbk6CkkRW8u3W4X29DIpt77Lq5Fux2u9XCSlsro14ArtWObQ</recordid><startdate>20090201</startdate><enddate>20090201</enddate><creator>Li, Suk-Yee</creator><creator>Fu, Zhong-Jie</creator><creator>Ma, Huan</creator><creator>Jang, Wai-Chi</creator><creator>So, Kwok-Fai</creator><creator>Wong, David</creator><creator>Lo, Amy C. Y</creator><general>ARVO</general><general>Association for Research in Vision and Ophtalmology</general><scope>IQODW</scope><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>20090201</creationdate><title>Effect of Lutein on Retinal Neurons and Oxidative Stress in a Model of Acute Retinal Ischemia/Reperfusion</title><author>Li, Suk-Yee ; Fu, Zhong-Jie ; Ma, Huan ; Jang, Wai-Chi ; So, Kwok-Fai ; Wong, David ; Lo, Amy C. Y</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c453t-2f9d9292f430e91103754a5ef9ae15ae7c23760d266ae45aaf37a19d2d110b783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Acute Disease</topic><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Calbindin 2</topic><topic>Cardiology. Vascular system</topic><topic>Disease Models, Animal</topic><topic>Eye and associated structures. Visual pathways and centers. Vision</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>In Situ Nick-End Labeling</topic><topic>Lutein - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Neurons - drug effects</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Ophthalmology</topic><topic>Oxidative Stress - drug effects</topic><topic>Poly Adenosine Diphosphate Ribose - metabolism</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Retinal Diseases - metabolism</topic><topic>Retinal Diseases - pathology</topic><topic>Retinal Diseases - prevention & control</topic><topic>Retinal Ganglion Cells - drug effects</topic><topic>Retinal Ganglion Cells - pathology</topic><topic>S100 Calcium Binding Protein G - metabolism</topic><topic>Tyrosine - analogs & derivatives</topic><topic>Tyrosine - metabolism</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Suk-Yee</creatorcontrib><creatorcontrib>Fu, Zhong-Jie</creatorcontrib><creatorcontrib>Ma, Huan</creatorcontrib><creatorcontrib>Jang, Wai-Chi</creatorcontrib><creatorcontrib>So, Kwok-Fai</creatorcontrib><creatorcontrib>Wong, David</creatorcontrib><creatorcontrib>Lo, Amy C. Y</creatorcontrib><collection>Pascal-Francis</collection><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>Investigative ophthalmology & visual science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Suk-Yee</au><au>Fu, Zhong-Jie</au><au>Ma, Huan</au><au>Jang, Wai-Chi</au><au>So, Kwok-Fai</au><au>Wong, David</au><au>Lo, Amy C. Y</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of Lutein on Retinal Neurons and Oxidative Stress in a Model of Acute Retinal Ischemia/Reperfusion</atitle><jtitle>Investigative ophthalmology & visual science</jtitle><addtitle>Invest Ophthalmol Vis Sci</addtitle><date>2009-02-01</date><risdate>2009</risdate><volume>50</volume><issue>2</issue><spage>836</spage><epage>843</epage><pages>836-843</pages><issn>0146-0404</issn><issn>1552-5783</issn><eissn>1552-5783</eissn><coden>IOVSDA</coden><abstract>Retinal ischemia/reperfusion (I/R) occurs in many ocular diseases and leads to neuronal death. Lutein, a potent antioxidant, is used to prevent severe visual loss in patients with early age-related macular degeneration (AMD), but its effect on I/R insult is unclear. The objective of the present study is to investigate the neuroprotective effect of lutein on retinal neurons after acute I/R injury.
Unilateral retinal I/R was induced by the blockade of internal carotid artery using intraluminal method in mice. Ischemia was maintained for 2 hours followed by 22 hours of reperfusion, during which either lutein or vehicle was administered. The number of viable retinal ganglion cells (RGC) was quantified. Apoptosis was investigated using TUNEL assay. Oxidative stress was elucidated using markers such as nitrotyrosine (NT) and poly(ADP-ribose) (PAR).
In vehicle-treated I/R retina, severe cell loss in ganglion cell layer, increased apoptosis as well as increased NT and nuclear PAR immunoreactivity were observed. In lutein-treated I/R retina, significantly less cell loss, decreased number of apoptotic cells, and decreased NT and nuclear PAR immunoreactivity were seen.
The neuroprotective effect of lutein was associated with reduced oxidative stress. Lutein has been hitherto used principally for protection of outer retinal elements in AMD. Our study suggests that it may also be relevant for the protection of inner retina from acute ischemic damage.</abstract><cop>Rockville, MD</cop><pub>ARVO</pub><pmid>18936152</pmid><doi>10.1167/iovs.08-2310</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Investigative ophthalmology & visual science, 2009-02, Vol.50 (2), p.836-843 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Acute Disease Animals Antioxidants - pharmacology Apoptosis Biological and medical sciences Calbindin 2 Cardiology. Vascular system Disease Models, Animal Eye and associated structures. Visual pathways and centers. Vision Fundamental and applied biological sciences. Psychology In Situ Nick-End Labeling Lutein - pharmacology Male Medical sciences Mice Mice, Inbred C57BL Neurons - drug effects Neuroprotective Agents - pharmacology Ophthalmology Oxidative Stress - drug effects Poly Adenosine Diphosphate Ribose - metabolism Reperfusion Injury - metabolism Reperfusion Injury - pathology Reperfusion Injury - prevention & control Retinal Diseases - metabolism Retinal Diseases - pathology Retinal Diseases - prevention & control Retinal Ganglion Cells - drug effects Retinal Ganglion Cells - pathology S100 Calcium Binding Protein G - metabolism Tyrosine - analogs & derivatives Tyrosine - metabolism Vertebrates: nervous system and sense organs |
| title | Effect of Lutein on Retinal Neurons and Oxidative Stress in a Model of Acute Retinal Ischemia/Reperfusion |
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