Protection of retinal function by sulforaphane following retinal ischemic injury

Ambrecht, Lindsay; Perlman, Jay I.; McDonnell, James F.; Zhai, Yougang; Qiao, Liang; Bu, Pengcheng

doi:10.1016/j.exer.2015.06.030

Cited by 16 publications

(7 citation statements)

References 21 publications

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“…Immediately prior to experimentation, the stock solution was diluted with sterile saline to a concentration of 50 mg/kg (final DMSO concentration 1%)3132. The pharmacological effects in vivo were examined using the following groups (n = 10 per group): (a) vehicle control, 0.5% carboxymethyl cellulose sodium salt (CMC) plus saline (containing 1% DMSO) administered once daily; (b) sulforaphane (50 mg/kg dissolved in saline (containing 1% DMSO)) injected intraperitoneally every other day; (c) rotenone (30 mg/kg rotenone suspended in 0.5% CMC) administered orally daily for 60 consecutive days; and (d) rotenone + sulforaphane, rotenone treatment orally alone or followed by sulforaphane injected intraperitoneally every other day.…”

Section: Methodsmentioning

confidence: 99%

Sulforaphane protects against rotenone-induced neurotoxicity in vivo: Involvement of the mTOR, Nrf2 and autophagy pathways

Zhou

Bin

Wang

et al. 2016

Sci Rep

125

105

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Sulforaphane, a naturally occurring compound found in cruciferous vegetables, has been shown to be neuroprotective in several neurological disorders. In this study, we sought to investigate the potential protective effects and associated molecular mechanisms of sulforaphane in an in vivo Parkinson’s disease (PD) model, based on rotenone-mediated neurotoxicity. Our results showed that sulforaphane inhibited rotenone-induced locomotor activity deficiency and dopaminergic neuronal loss. Additionally, sulforaphane treatment inhibited the rotenone-induced reactive oxygen species production, malondialdehyde (MDA) accumulation, and resulted in an increased level of total glutathione and reduced glutathione (GSH): oxidized glutathione (GSSG) in the brain. Western blot analysis illustrated that sulforaphane increased the expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2), heme oxygenase-1 (HO-1), and NAD(P)H quinone oxidoreductase (NQO1), the latter two of which are anti-oxidative enzymes. Moreover, sulforaphane treatment significantly attenuated rotenone-inhibited mTOR-mediated p70S6K and 4E-BP1 signalling pathway, as well as neuronal apoptosis. In addition, sulforaphane rescued rotenone-inhibited autophagy, as detected by LC3-II. Collectively, these findings demonstrated that sulforaphane exert neuroprotective effect involving Nrf2-dependent reductions in oxidative stress, mTOR-dependent inhibition of neuronal apoptosis, and the restoration of normal autophagy. Sulforaphane appears to be a promising compound with neuroprotective properties that may play an important role in preventing PD.

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Section: Methodsmentioning

confidence: 99%

Sulforaphane protects against rotenone-induced neurotoxicity in vivo: Involvement of the mTOR, Nrf2 and autophagy pathways

Zhou

Bin

Wang

et al. 2016

Sci Rep

125

105

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“…(9) In some previous studies, SFN showed therapeutic effects on neural protection, and could protect brains against hypoxic-ischemic injury(10) and relieve ischemia-reperfusion-induced retinal damage. (11,12) Our study investigated the protective effects of SFN on retinal photoreceptor cells in rd10 mice, which provides data for further developing SFN as a new therapeutic medication for RP.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of sulforaphane against retinal degeneration in the Pde6^rd10 mouse model of retinitis pigmentosa

Kang

2017

Current Eye Research

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Purpose Retinitis pigmentosa (RP), a group of inherited diseases characterized by the death of rod photoreceptors, followed by the death of cone photoreceptors, progressively leading to partial or complete blindness. Currently no specific treatment is available for RP patients. Sulforaphane (SFN) has been confirmed to be an effective antioxidant in the treatment of many diseases. In this study, we tested the therapeutic effects of SFN against photoreceptor degeneration in Pde6rd10 (rd10) mice. Methods rd10 mice and C57BL/6J wild-type (WT) mice were treated with SFN and saline, respectively, from P6 to P20. Electroretinography (ERG), terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and western blot were tested, respectively, at P21 for the analysis of retinal function, retinal cell apoptosis or death and the protein express of GRP78/BiP (TUNEL) as a marker of endoplasmic reticulum stress. Results Compared to the saline group, the SFN-treated group showed significantly higher ERG a-wave and b-wave amplitudes, less photoreceptor death, and downregulation of GRP78/BiP. Conclusions Our data showed that SFN ameliorated the retinal degeneration of rd10 mice, which is possibly related to the downregulation of GRP78 expression.

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“…Supporting previous results, in 2015 [124], a new work was published, in which the authors administered SFN to a mice model of retinal ischemia-reperfusion, but this time the SFN concentration and time administration were found to be higher and shorter, respectively. The morphological retinal alterations, thinning of the inner retinal layer, and the dysfunction activity of the retina, measured by scotopic electroretinography, were reverted by SFN, specifically, the a and b waves amplitudes showed in a significant reduction in the control mice and was slightly reverted by the SFN.…”

Section: Sulforaphane As Antioxidant Treatment In Retinal Diseasesmentioning

confidence: 54%

Progesterone, Lipoic Acid, and Sulforaphane as Promising Antioxidants for Retinal Diseases: A Review

2019

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Oxidative stress has been documented to be a key factor in the cause and progression of different retinal diseases. Oxidative cellular unbalance triggers a sequence of reactions which prompt cell degeneration and retinal dysfunction, both hallmarks of several retinal pathologies. There is no effective treatment, yet, for many retinal diseases. Antioxidant treatment have been pointed out to be an encouraging palliative treatment; the beneficial effects documented involve slowing the progression of the disease, a reduction of cell degeneration, and improvement of retinal functions. There is a vast information corpus on antioxidant candidates. In this review, we expose three of the main antioxidant treatments, selected for their promising results that has been reported to date. Recently, the sulforaphane, an isothiocyanate molecule, has been unveiled as a neuroprotective candidate, by its antioxidant properties. Progesterone, a neurosteroid has been proposed to be a solid and effective neuroprotective agent. Finally, the lipoic acid, an organosulfur compound, is a well-recognized antioxidant. All of them, have been tested and studied on different retinal disease models. In this review, we summarized the published results of these works, to offer a general view of the current antioxidant treatment advances, including the main effects and mechanisms described.

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Protection of retinal function by sulforaphane following retinal ischemic injury

Cited by 16 publications

References 21 publications

Sulforaphane protects against rotenone-induced neurotoxicity in vivo: Involvement of the mTOR, Nrf2 and autophagy pathways

Sulforaphane protects against rotenone-induced neurotoxicity in vivo: Involvement of the mTOR, Nrf2 and autophagy pathways

Protective effect of sulforaphane against retinal degeneration in the Pde6^rd10 mouse model of retinitis pigmentosa

Progesterone, Lipoic Acid, and Sulforaphane as Promising Antioxidants for Retinal Diseases: A Review

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Protection of retinal function by sulforaphane following retinal ischemic injury

Cited by 16 publications

References 21 publications

Sulforaphane protects against rotenone-induced neurotoxicity in vivo: Involvement of the mTOR, Nrf2 and autophagy pathways

Sulforaphane protects against rotenone-induced neurotoxicity in vivo: Involvement of the mTOR, Nrf2 and autophagy pathways

Protective effect of sulforaphane against retinal degeneration in the Pde6rd10 mouse model of retinitis pigmentosa

Progesterone, Lipoic Acid, and Sulforaphane as Promising Antioxidants for Retinal Diseases: A Review

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Protective effect of sulforaphane against retinal degeneration in the Pde6^rd10 mouse model of retinitis pigmentosa