The therapeutic potential of sulforaphane on light-induced photoreceptor degeneration through antiapoptosis and antioxidant protection

Kong, Li; Liu, Bo; Zhang, Chenghong; Wang, Bing; Hong-fei, Wang; Song, Xiaoxia; Yang, Yang; Ren, Xiang; Yin, Liangwei; Kong, Hui; Ma, Haiying

doi:10.1016/j.neuint.2016.08.011

Cited by 15 publications

(9 citation statements)

References 55 publications

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“…The other genes analyzed by PCR were related to the inflammation response. Three years later, in 2016 [113], an in vivo research on retinal photooxidation showed a set of results which confirmed the increased expression of Nrf2 and Trx1 by SFN, but also, showed that the anti-caspase activity was added to the antioxidant activity elicited by SFN. For more details on these treatments, please see Table 3.…”

Section: Sulforaphane As Antioxidant Treatment In Retinal Diseasesmentioning

confidence: 99%

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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Section: Sulforaphane As Antioxidant Treatment In Retinal Diseasesmentioning

confidence: 99%

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

2019

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“…Moreover, Previous studies have shown that SF can up-regulate Trx [18] and that SF treatment inhibits retinal degeneration in Tubby mice [19]. It indicated that Trx might play an important role in fighting against the retina degeneration process.…”

Section: Introductionmentioning

confidence: 98%

Up-Regulation Thioredoxin Inhibits Advanced Glycation End Products-Induced Neurodegeneration

Ren

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Diabetic retinopathy (DR) is one of the most serious complications of diabetes and is the leading cause of adult blindness in developed countries. Advanced glycation end products (AGEs) accumulation in diabetes is associated with its complications. Thioredoxin (Trx) is a small molecule (12kDa) antioxidant protein widely distributed in mammalian tissues, which has important biological functions including anti-apoptosis and transcriptional regulation. In a previous study, we found that Trx plays a key role in retinal neurodegeneration prior to the occurrence of endothelial damage in diabetic mice. In this study, our aim is to determine the effect of Trx on neurodegeneration induced by AGEs in order to identify new therapeutic targets for the clinical treatment and prevention of DR. Methods: In vivo, a high-fat diet and Streptozotocin (STZ) injection were used to generate a mouse model of diabetes. Histology was utilized to examine tissue morphology and measure the outer nuclear layer (ONL) thickness. Electroretinography (ERG) was used to assess retinal function and Western blot was used to examine protein expression. In vitro, three methods of Trx up-regulation were used, including a stable cell line that overexpresses Trx, treatment with Sulforaphane, and shRNA down-regulation Txnip. Cells were treated with AGEs, and level of apoptosis was performed to quantify this by flow cytometry and TUNEL. Quantitative Reverse Transcription PCR (qRT-PCR), Western blotting and immunofluorescence were used to measure gene and protein expression. Transmission electron microscopy (TEM) was used to observe autophagosomes. Results: We found that diabetic mice display decreased retinal function and reduced ONL thickness with AGEs accumulation and a reduction of Trx expression. Up-regulation Trx can prevent the ONL thickness decrease in diabetic mice, as observed by H&E staining. In vitro, up-regulation Trx resulted in decreased intracellular ROS generation, reduced apoptosis by inhibited autophagy. Conclusion: Up-regulating Trx inhibited neurodegeneration induced by AGEs. The underlying mechanism may be related to inhibit Txnip/mTOR pathway-mediated autophagy.

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“…Light is the ultimate powerful agent for the maintenance of circadian clocks. However, prolonged exposure to artificial light disturbs circadian rhythms (1,2) and leads to retinal degeneration, such as macular degeneration and retinitis pigmentosa, which is associated with photoreceptor degeneration (3). Prolonged exposure to bright light mediates photoreceptor cell death, which is an irrevocable retinal disorder and causes impaired vision function, vision loss or blindness (4,5).…”

Section: Introductionmentioning

confidence: 99%

“…Excessive light exposure promotes a cascade of oxidative stress-associated events involved in retinal degeneration (6,7), which serves a pivotal role in accelerating several degenerative diseases such as age-related macular degeneration (AMD) and retinitis pigmentosa (RP) (3). Overproduction of reactive oxygen species (ROS) can lead to retinal functional and morphological changes that result in vision impairment (8,9).…”

Section: Introductionmentioning

confidence: 99%

Ginkgo biloba delays light‑induced photoreceptor degeneration through antioxidant and antiapoptotic properties

et al. 2021

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Intense exposure to artificial bright light increases the risk of retinal damage resulting in blurred vision and blindness. Long-term exposure to bright light elevates oxidative stress-induced apoptosis, which results in photoreceptor cell degeneration. However, to the best of our knowledge, the molecular mechanism associated with light-induced retinopathy remains unclear. In the present study, the mechanisms involved in light-induced oxidative stress and apoptosis were investigated along with the protective effects of Ginkgo biloba (EGb 761) in photoreceptor cell degeneration. EGb 761 was administered to mice at a dose of 50 or 100 mg/kg for 7 days prior to exposure to bright light (5,000 lux for 24 h). Furthermore, photoreceptor cell disorders were evaluated using electroretinogram (ERG) and H&E staining analyses. The expression levels of antioxidant genes and proteins ERK, thioredoxin (Trx) and nuclear factor erythroid 2-related factor 2 (Nrf-2) and the induction of apoptosis cytochrome c (Cyc), cleaved caspase-3 and Bax, were determined by reverse transcription-quantitative PCR and western blotting. ERG and histological analysis revealed that exposure to bright light induced functional and morphological changes to the photoreceptor cells. Exposure to bright light increased the levels of Cyc, cleaved caspase-3 and Bax, and decreased the levels of phosphorylated (p-) Erk, Nrf-2 and thioredoxin (Trx). However, treatment of mice with EGb 761 increased the expression levels of antiapoptotic (Bcl-2) and antioxidant (p-Erk, Trx and Nrf-2) proteins and decreased the expression levels of the apoptotic genes (Cyc, cleaved caspase-3 and Bax). Based on these findings, the present study suggested that prolonged exposure to light induces photoreceptor cell degeneration, where EGb 761 treatment may serve a therapeutic effect on the development of photoreceptor cell degeneration.

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The therapeutic potential of sulforaphane on light-induced photoreceptor degeneration through antiapoptosis and antioxidant protection

Cited by 15 publications

References 55 publications

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

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

Up-Regulation Thioredoxin Inhibits Advanced Glycation End Products-Induced Neurodegeneration

Ginkgo biloba delays light‑induced photoreceptor degeneration through antioxidant and antiapoptotic properties

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