{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T15:52:25Z","timestamp":1777909945810,"version":"3.51.4"},"reference-count":33,"publisher":"SAGE Publications","issue":"8","license":[{"start":{"date-parts":[[2021,10,1]],"date-time":"2021-10-01T00:00:00Z","timestamp":1633046400000},"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":[[2021,10,1]]},"abstract":"<jats:sec>\n                    <jats:title>Purpose:<\/jats:title>\n                    <jats:p>Retinal ischemia\/reperfusion (I\/R) injury is a common cause of visual impairment and blindness for which there remain limited treatment options. Nucleoside reverse transcriptase inhibitors (NRTIs), such as zidovudine (AZT), have been shown to block the NLRP3 inflammasome and prevent retinal degeneration in a mouse model of age-related macular degeneration. The NLRP3 inflammasome has also been shown to be triggered in I\/R injury. Therefore, we studied the neuroprotective effects of AZT using a pressure-induced retinal ischemia mouse model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      C57BL\/6J mice were randomly assigned to 1 of 2 treatment groups: vehicle-treated retinal I\/R injury (\n                      <jats:italic toggle=\"yes\">n<\/jats:italic>\n                      \u2009=\u20096) or AZT-treated retinal I\/R injury (\n                      <jats:italic toggle=\"yes\">n<\/jats:italic>\n                      \u2009=\u20096). Vehicle (1% dimethyl sulfoxide [DMSO] in phosphate-buffered saline [PBS]) or AZT 50\u2009mg\/kg in 1% DMSO in PBS were injected intraperitoneally twice daily for 5 days. On day 2 of treatment, retinal ischemia was induced by transient elevation of intraocular pressure for 45\u2009min. Scotopic electroretinography (ERG) was used to quantify retinal function before and 1 week after retinal ischemic insult. Retinal morphology was examined 1 week after ischemic insult. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assays and caspase 1 immunostaining was performed 24\u2009h after retinal I\/R injury.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>Following I\/R injury, ERG a- and b-wave amplitudes were significantly reduced in the vehicle-treated mice. AZT treatment significantly attenuated I\/R-induced loss of retinal function as compared with vehicle-treated mice. Additionally, AZT-treated mice experienced significantly less inner retinal thinning as compared with vehicle-treated mice. TUNEL-positive cells were prevalent in the vehicle-treated I\/R injury mouse retinas compared with the AZT-treated I\/R injury mouse retinas. More caspase-1 immunoreactivity was detected in ganglion cell layer and inner nuclear layer (INL) in vehicle-treated I\/R injury group than in AZT-treated I\/R injury group.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>AZT treatment resulted in relative preservation of retinal structure and function following ischemic insult as compared with controls. This suggests AZT may have therapeutic value in the management of retinal ischemic diseases.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1089\/jop.2020.0083","type":"journal-article","created":{"date-parts":[[2021,8,27]],"date-time":"2021-08-27T11:57:14Z","timestamp":1630065434000},"page":"485-491","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":4,"title":["Protection of Retinal Function by Nucleoside Reverse Transcriptase Inhibitors Following Retinal Ischemia\/Reperfusion Injury"],"prefix":"10.1177","volume":"37","author":[{"given":"William S.","family":"Gange","sequence":"first","affiliation":[{"name":"Health Sciences Division, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James B.","family":"Qiao","sequence":"additional","affiliation":[{"name":"Health Sciences Division, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul J.","family":"Park","sequence":"additional","affiliation":[{"name":"Health Sciences Division, Department of Ophthalmology, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James F.","family":"McDonnell","sequence":"additional","affiliation":[{"name":"Health Sciences Division, Department of Ophthalmology, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhiqun","family":"Tan","sequence":"additional","affiliation":[{"name":"Institute for Neurological Impairments and Neurological Disorders, University of California Irvine, Irvine, California, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jay I.","family":"Perlman","sequence":"additional","affiliation":[{"name":"Health Sciences Division, Department of Ophthalmology, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois, USA."},{"name":"Surgery Service and Edward Hines Jr. VA Hospital, Hines, Illinois, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3526-1326","authenticated-orcid":false,"given":"Ping","family":"Bu","sequence":"additional","affiliation":[{"name":"Health Sciences Division, Department of Ophthalmology, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois, USA."},{"name":"Research Service, Edward Hines Jr. VA Hospital, Hines, Illinois, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2021,10,4]]},"reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.preteyeres.2003.12.001"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1001\/archopht.1975.01010020934002"},{"key":"e_1_3_4_4_2","first-page":"54065","article-title":"A mouse model of retinal ischemia-reperfusion injury through elevation of intraocular pressure","volume":"113","author":"Hartsock M.J.","year":"2016","unstructured":"Hartsock M.J., , Cho H., , Wu L., , Chen W.J., , Gong J., , and Duh E.J. A mouse model of retinal ischemia-reperfusion injury through elevation of intraocular pressure. J. Vis. Exp. 113:54065, 2016.","journal-title":"J. Vis. 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