Diosmin protects rat retina from ischemia/reperfusion injury.

Content Provider	Europe PMC
Author	Tong, Nianting Zhang, Zhenzhen Gong, Yuanyuan Yin, Lili Wu, Xingwei
Copyright Year	2012
Abstract	Abstract Objective 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. Methods Retinal I/R injury was induced in the rats by elevating the IOP to 110 mmHg for 60 min. Diosmin (100 mg/kg) or vehicle solution was administered intragastrically 30 min 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 h 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. Results 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 (P<0.05), and suppressed the I/R-induced reduction in the a- and b-wave amplitudes of the ERG (P<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 (P<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 (P<0.05). Conclusion Diosmin protected the retina from I/R injury, possibly via a mechanism involving the regulation of oxidative parameters.
Related Links	https://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC3459007&blobtype=pdf
Page Count	8
ISSN	10807683
Volume Number	28
DOI	10.1089/jop.2011.0218
PubMed Central reference number	PMC3459007
Issue Number	5
PubMed reference number	22509733
Journal	Journal of Ocular Pharmacology and Therapeutics [J Ocul Pharmacol Ther]
e-ISSN	15577732
Language	English
Publisher	Mary Ann Liebert, Inc.
Publisher Date	2012-04-17
Publisher Place	USA
Access Restriction	Open
Rights License	Copyright 2012, Mary Ann Liebert, Inc.
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Pharmacology Pharmacology (medical)