{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T15:48:10Z","timestamp":1777909690634,"version":"3.51.4"},"reference-count":43,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[2012,4,17]],"date-time":"2012-04-17T00:00:00Z","timestamp":1334620800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Ocular Pharmacology and Therapeutics"],"published-print":{"date-parts":[[2012,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>Diosmin, a natural flavone glycoside, possesses antioxidant activity and has been used to alleviate ischemia\/reperfusion (I\/R) injury. The aim of this study was to clarify whether the administration of diosmin has a protective effect against I\/R injury induced using the high intraocular pressure (IOP) model in rat retina, and to determine the possible antioxidant mechanisms involved.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Retinal I\/R injury was induced in the rats by elevating the IOP to 110\u2009mmHg for 60\u2009min. Diosmin (100\u2009mg\/kg) or vehicle solution was administered intragastrically 30\u2009min before the onset of ischemia and then daily after I\/R injury until the animals were sacrificed. The levels of malondialdehyde (MDA) and the activities of total-superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in the retinal tissues were determined 24\u2009h after I\/R injury. At 7 days post-I\/R injury, electroretinograms (ERGs) were recorded, and the density of surviving retinal ganglion cells (RGCs) was estimated by counting retrograde tracer-labeled cells in whole-mounted retinas. Retinal histological changes were also examined and quantified using light microscopy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      Diosmin significantly decreased the MDA levels and increased the activities of T-SOD, GSH-Px, and CAT in the retina of rats compared with the ischemia group (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.05), and suppressed the I\/R-induced reduction in the a- and b-wave amplitudes of the ERG (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.05). The thickness of the entire retina, inner nuclear layer, inner plexiform layer, and outer retinal layer and the number of cells in the ganglion cell layer were significantly less after I\/R injury (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.05), and diosmin remarkably ameliorated these changes on retinal morphology. Diosmin also attenuated the I\/R-induced loss of RGCs of the rat retina (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>Diosmin protected the retina from I\/R injury, possibly via a mechanism involving the regulation of oxidative parameters.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/jop.2011.0218","type":"journal-article","created":{"date-parts":[[2012,4,17]],"date-time":"2012-04-17T12:45:22Z","timestamp":1334666722000},"page":"459-466","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":31,"title":["Diosmin Protects Rat Retina from Ischemia\/Reperfusion Injury"],"prefix":"10.1177","volume":"28","author":[{"given":"Nianting","family":"Tong","sequence":"first","affiliation":[{"name":"Shanghai Jiaotong University Affiliated Shanghai First People's Hospital","place":["China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhenzhen","family":"Zhang","sequence":"additional","affiliation":[{"name":"Shanghai Jiaotong University Affiliated Shanghai First People's Hospital","place":["China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuanyuan","family":"Gong","sequence":"additional","affiliation":[{"name":"Shanghai Jiaotong University Affiliated Shanghai First People's Hospital","place":["China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lili","family":"Yin","sequence":"additional","affiliation":[{"name":"Shanghai Jiaotong University Affiliated Shanghai First People's Hospital","place":["China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xingwei","family":"Wu","sequence":"additional","affiliation":[{"name":"Shanghai Jiaotong University Affiliated Shanghai First People's Hospital","place":["China"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2012,4,17]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.preteyeres.2003.12.001"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1992.tb08912.x"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1097\/00061198-199802000-00012"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1167\/iovs.08-2310"},{"key":"e_1_3_3_6_2","first-page":"337","article-title":"Oxygen free radicals and the gastrointestinal tract: role in ischemia-reperfusion injury","volume":"41","author":"Zimmerman B.J.","year":"1994","unstructured":"Zimmerman B.J., , Granger D.N. 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