Suppression of Laser-Induced Choroidal Neovascularization by Posterior Sub-Tenon Administration of Triamcinolone Acetonide

Kato, Aki; Kimura, Hideya; Okabe, Komei; Okabe, Junko; Kunou, Noriyuki; Nozaki, Miho; Ogura, Yuichiro

doi:10.1097/00006982-200506000-00017

Cited by 22 publications

(15 citation statements)

References 37 publications

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“…Next, 100 l of the supernatant was added to 200 l of ethyl acetate, vortexed for 2 min, centrifuged at 13,000 rpm for 5 min, and 20 l of supernatant was collected. As described in a previous report [15] , high-performance liquid chromatography was used to measure the vitreoretinal U83836E level in diabetic rats.…”

Section: High-performance Liquid Chromatographymentioning

confidence: 99%

U83836E Inhibits Retinal Neurodegeneration in Early-Stage Streptozotocin-Induced Diabetic Rats

Wang¹,

Zheng²,

Gong³

et al. 2010

Ophthalmic Res

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Oxidative stress plays a role in the pathogenesis of neurodegeneration in diabetic retinopathy (DR). However, whether an excellent reactive oxygen species scavenger, U83836E, inhibits the neurodegeneration in DR remains uncertain. This study is aimed at clarifying the effects of U83836E on DR. Two weeks after streptozotocin (STZ) injection, diabetic rats and control animals were assigned at random to receive U83836E or vehicle for 2 weeks. Transmission electron microscopy and electroretinography were used to observe the changes in retina ultrastructure and electrophysiological function, respectively; superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were measured using a spectrometer. STZ-induced diabetic rats showed obvious vacuolation and many swollen mitochondria in the retinal ganglion cells of the retina, and reduced amplitudes of b-waves and oscillatory potentials. Concomitantly, there was a decrease in SOD activity and increase in MDA levels. These changes were inhibited by U83836E. These results suggest that U83836E improves neurodegeneration in DR and possesses a great potential for the treatment of DR.

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Section: High-performance Liquid Chromatographymentioning

confidence: 99%

U83836E Inhibits Retinal Neurodegeneration in Early-Stage Streptozotocin-Induced Diabetic Rats

Wang¹,

Zheng²,

Gong³

et al. 2010

Ophthalmic Res

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“…Animal models could provide us with data about the earliest phases of CNV development. So far the preferred way of CNV induction in different treatment trials has been by laser [16,31] but this method also causes retinal tissue destruction [5,17,24] which makes it complicated to determine whether damage to the neuroretina is caused by the process of CNV formation or by the laser burn. Reliable animal models with a bearing to human clinic are also essential in order to test the effect of new treatment modalities such as antiangiogenic therapy.…”

Section: Introductionmentioning

confidence: 99%

Surgical induction of choroidal neovascularization in a porcine model

Lassota

Kiilgaard

Prause

et al. 2007

Graefes Arch Clin Exp Ophthalmol

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“…Macugen is injected intravitreally every six weeks and there are reports of increased complications associated with repeated injections (eight times per year) for one year (Gragoudas et al 2004), but the long term effects of repeated intravitreal injections are still unknown. In this study, we have compared the efficacy of intravitreal versus intraperitoneal injections, but other delivery routes are also possible (Okada et al, 2004;Augustin et al, 2005;Kato et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Receptor tyrosine kinase inhibitors AG013764 and AG013711 reduce choroidal neovascularization in rat eye

Wang

Shi

Niesman

et al. 2007

Experimental Eye Research

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Age-related macular degeneration (AMD) is the major cause of blindness for people over 60. In the "wet" form of AMD compounds targeting growth factor signaling pathways such as VEGF have been a major focus for therapeutic interventions. In a previously developed rat model of CNV, we utilized two receptor tyrosine kinase inhibitors (RTKi) to block VEGFR-1, VEGFR-2 and PDGFR signaling following the establishment of CNV. AAV-VEGF 165 was injected into the subretinal space of rats at postnatal days 15-17. Six weeks later, a suspension of RTK inhibitors, AG013764 or AG013711, was injected intraperitoneally (IP, twice daily) or intravitreally (every five days) over a two week period. FITC-dextran whole-mounts of RPE-choroid-sclera were prepared after the animals were sacrificed. CNV area was quantified using Neurolucida to measure the hyperfluorescence on FITC-dextran whole-mounts. Histology and immunohistochemistry were performed as described previously. VEGF expression in control and treated eyes was confirmed by immunohistochemistry and histological sections indicated recovery of retinal morphology and CNV reduction in treated eyes. In the animals IP injected with AG013764 or AG013711 the mean CNV level was reduced by 25 to 33% compared to control, but this effect did not achieve statistical significance. Intravitreal injections of AG013764 or AG013711 reduced the level of CNV by approximately 60% compared to control (p< 0.005 or p< 0.05, respectively). These data show that two RTK inhibitors, AG013764 or AG013711, delivered intravitreally, significantly reduce blood vessel proliferation in this AAV-VEGF 165 model of CNV.

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Suppression of Laser-Induced Choroidal Neovascularization by Posterior Sub-Tenon Administration of Triamcinolone Acetonide

Abstract: Posterior sub-Tenon administration of TA may be useful to treat CNV.

Cited by 22 publications

References 37 publications

U83836E Inhibits Retinal Neurodegeneration in Early-Stage Streptozotocin-Induced Diabetic Rats

U83836E Inhibits Retinal Neurodegeneration in Early-Stage Streptozotocin-Induced Diabetic Rats

Surgical induction of choroidal neovascularization in a porcine model

Receptor tyrosine kinase inhibitors AG013764 and AG013711 reduce choroidal neovascularization in rat eye

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