In vivo and in vitro experiments show that betaxolol is a retinal neuroprotective agent

Osborne, Neville N.; Cazevieille, Chantal; Carvalho, Ana Luı́sa; Larsen, Axel; DeSantis, Louis

doi:10.1016/s0006-8993(96)01393-5

Cited by 109 publications

(63 citation statements)

References 30 publications

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“…Betaxolol is a selective b 1-adrenergic blocker, but its neuroprotective action is generally thought to be due to its calcium channel blocking properties (8,12). We can not exclude the possibility that the selective b 1-adrenergic blocking property of betaxolol is may be related to this neuroprotective effect in this study.…”

Section: Discussionmentioning

confidence: 76%

“…We can not exclude the possibility that the selective b 1-adrenergic blocking property of betaxolol is may be related to this neuroprotective effect in this study. However, it is reported that a b -adrenergic receptor antagonist such as timolol has no neuroprotective effect on NMDA-induced retinal injury (35) and that betaxolol has a greater L-type blocking activity than other b -adrenergic receptor antagonist (36) and neuroprotective effect on the ischemiainduced retinal injury (12,13). These results suggested that betaxolol may function as a neuroprotective agent by reducing the excessive influx of calcium into the cell in some way (see the Introduction).…”

Section: Discussionmentioning

confidence: 99%

“…However, some b-adrenergic antagonists have also been shown to act as calcium channel antagonists (7 -11). Betaxolol is a selective b1-adrenergic blocker, but its neuroprotective action is generally thought to be due to its calcium channel blocking properties (8,12). Betaxolol also blunted the ischemia-induced damages, more precisely N-methyl-Daspartate (NMDA) toxicity (13).…”

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confidence: 99%

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Effect of Betaxolol on Aspartate Aminotransferase Activity in Hypoxic Rat Retina In Vitro

Endo

Tomita

Ishiguro

et al. 2002

Japanese Journal of Pharmacology

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ABSTRACT-We investigated the effect of betaxolol on the decrease of mitochondrial aspartate aminotransferase (mAAT) activity in rat retinas induced by hypoxia in vitro. It is reported that mAAT decreases in ischemic or hypoxic retina and that the decrease is caused by Ca 2+ -dependent proteases such as calpain. Betaxolol is a compound that has b1-adrenergic receptor blocking and voltage-dependent calcium channel blocking properties. The rat eye cups were maintained with Locke's solution saturated with 95% air -5% CO2. The eye cups were immersed in glucose-free Locke's solution saturated with 95% N2 / 5% CO2 (hypoxic solution). Ninety minutes of hypoxia caused a 20% decrease in mAAT activity. The eye cups incubated with the hypoxic solution containing 1 mM EGTA, 10 mM MK-801 or 100 mM betaxolol were protected from the decrease in mAAT activity, so that the residual mAAT activity was 50%, 45% or 40%, respectively, compared to the eye cups incubated in hypoxic solution alone, which had a 100% decrease in mAAT activity. In addition, co-incubation with EGTA and betaxolol had a greater protective effect against the mAAT decrease than a single application. This additive effect of betaxolol was dose-dependent. These results suggested that betaxolol had a protective effect against the decrease of mAAT caused by hypoxia and indicated that betaxolol might inhibit the Ca 2+ release from intracellular Ca 2+ stores.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Effect of Betaxolol on Aspartate Aminotransferase Activity in Hypoxic Rat Retina In Vitro

Endo

Tomita

Ishiguro

et al. 2002

Japanese Journal of Pharmacology

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“…Several in vitro studies have demonstrated the neuroprotective effects of betaxolol at relatively high concentrations. [49][50][51][52] However, it remains to be clarified whether topically applied betaxolol reaches the retina or optic nerve head in human eyes at the effective concentrations reported in the in vitro studies.…”

Section: Discussionmentioning

confidence: 99%

Influence of Topical Betaxolol and Timolol on Visual Field in Japanese Open-angle Glaucoma Patients

Araie

2003

Japanese Journal of Ophthalmology

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“…Recently, some of the antiglaucoma drugs have shown neuroprotective effects against ischemic retinal damage (specially inner retina) and optic nerve injury [1,2]. Are there any protective effects on photoreceptor or outer retina by antiglaucoma drugs?…”

Section: Introductionmentioning

confidence: 99%

Photoreceptor Protection against Constant Light-Induced Damage by Isopropyl Unoprostone, a Prostaglandin F<sub>2α</sub> Metabolite-Related Compound

Hayami

Unoki²

2001

Ophthalmic Res

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Some of the antiglaucoma drugs have shown neuroprotective effects in ischemic retinal damage and optic nerve injury. We studied photoreceptor protection against constant light-induced damage using isopropyl unoprostone, a prostaglandin F_2α metabolite-related compound. Albino Sprague-Dawley rats were administered isopropyl unoprostone solution intravitreally in one eye (the test eye) and vehicle alone in the contralateral eye (the control eye) and were exposed to constant light for 7 days. Histological examinations were performed to evaluate photoreceptor protection by quantifying the outer nuclear layer (ONL) thickness and scoring the rescue of ONL. Seven-day constant light affected photoreceptors and produced a marked disruption of photoreceptor outer segments and inner segments and a decrease in the thickness of the ONL. As compared with control eyes, pretreatment by intravitreal administration of isopropyl unoprostone 2 days prior to constant light exposure provided protection from the light insult, and the effects of rescue were dependent on the dose of the agent (0.6–6.0 µg), the maximum dose protecting about 70% of the photoreceptors. Topical application of the drug had little rescue effect. Aberrant macrophages in light-exposed eyes with unoprostone injection were more numerous than in normal eyes, but the extent did not differ significantly from that of degenerated eyes injected with vehicle only. Isopropyl unoprostone has shown protection of photoreceptors against constant light-induced damage, and it is thus suggested that the agent has neuroprotective activity in vivo.

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In vivo and in vitro experiments show that betaxolol is a retinal neuroprotective agent

Cited by 109 publications

References 30 publications

Effect of Betaxolol on Aspartate Aminotransferase Activity in Hypoxic Rat Retina In Vitro

Effect of Betaxolol on Aspartate Aminotransferase Activity in Hypoxic Rat Retina In Vitro

Influence of Topical Betaxolol and Timolol on Visual Field in Japanese Open-angle Glaucoma Patients

Photoreceptor Protection against Constant Light-Induced Damage by Isopropyl Unoprostone, a Prostaglandin F<sub>2α</sub> Metabolite-Related Compound

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