Department of Ophthalmology, Shanghai Jiaotong University Affiliated Shanghai First People's Hospital, Shanghai, China.
J Ocul Pharmacol Ther. 2012 Oct;28(5):459-66. doi: 10.1089/jop.2011.0218. Epub 2012 Apr 17.
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.
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.
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).
Diosmin protected the retina from I/R injury, possibly via a mechanism involving the regulation of oxidative parameters.
地奥司明是一种天然黄酮苷类化合物，具有抗氧化活性，已被用于减轻缺血/再灌注（I/R）损伤。本研究旨在阐明地奥司明对大鼠视网膜高眼压（IOP）模型诱导的 I/R 损伤是否具有保护作用，并确定可能涉及的抗氧化机制。
通过将 IOP 升高至 110mmHg 持续 60min 诱导视网膜 I/R 损伤。地奥司明（100mg/kg）或载体溶液在缺血前 30min 经胃内给药，然后在 I/R 损伤后每天给药，直至动物处死。在 I/R 损伤后 24h 测定视网膜组织中丙二醛（MDA）水平和总超氧化物歧化酶（T-SOD）、谷胱甘肽过氧化物酶（GSH-Px）和过氧化氢酶（CAT）的活性。在 I/R 损伤后 7 天，记录视网膜电图（ERG），并通过计数整个视网膜中逆行示踪剂标记的细胞来估计存活的视网膜神经节细胞（RGC）的密度。还通过光镜检查和量化视网膜组织学变化。
与缺血组相比，地奥司明显著降低了大鼠视网膜 MDA 水平，增加了 T-SOD、GSH-Px 和 CAT 的活性（P<0.05），并抑制了 I/R 诱导的 ERG 的 a-和 b-波幅度降低（P<0.05）。整个视网膜、内核层、内丛状层和外视网膜层的厚度以及节细胞层中的细胞数量在 I/R 损伤后显著减少（P<0.05），地奥司明显著改善了这些视网膜形态的变化。地奥司明还减轻了 I/R 诱导的大鼠视网膜 RGC 丢失（P<0.05）。
地奥司明可保护视网膜免受 I/R 损伤，其机制可能涉及氧化参数的调节。
