sulforaphane/atrofija

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Delay of photoreceptor degeneration in tubby mouse by sulforaphane.

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In this study, the homozygous tubby (tub/tub) mutant mouse, with an early progressive hearing loss and photoreceptor degeneration, was used as a model system to examine the effects of systemic administration of a naturally occurring isothiocyanate, sulforaphane (SF), on photoreceptor degeneration.

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

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Oxidative stress due to excessive light exposure can exacerbate a variety of human retinal diseases by accelerating photoreceptor cell death. The thioredoxin (Trx) system is considered to play a crucial role in reduction/oxidation (redox) regulation of signal transduction and in cell defense against

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

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Retinitis pigmentosa (RP) is 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

Sulforaphane ameliorates serum starvation-induced muscle atrophy via activation of the Nrf2 pathway in cultured C2C12 cells.

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Oxidative stress, an imbalance of redox homeostasis, contributes to the pathogenesis and progress of muscle atrophy. However, it is debated whether oxidative stress is a cause or consequence of muscle atrophy. In this study, we investigated the relationship between menadione-induced oxidative stress

Sulforaphane delays diabetes-induced retinal photoreceptor cell degeneration

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Diabetic retinopathy (DR) is a serious neurodegenerative disease that is induced by hyperglycaemia. Oxidative stress, inflammation and endoplasmic reticulum (ER) stress are involved in the development of DR. Sulforaphane (SF) is widely found in cruciferous plants and has a protective effect against

Molecular mechanisms underlying cochlear degeneration in the tubby mouse and the therapeutic effect of sulforaphane.

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As with Usher syndrome observed in humans, the two main phenotypes of the tubby mouse are progressive hearing loss and retinal degeneration. Yet, the mechanism underlying the tub-related cochlear degeneration is still unclear. The reduction/oxidation (redox) imbalance in the cell is related to many

L-Sulforaphane Confers Protection Against Oxidative Stress in an In Vitro Model of Age-Related Macular Degeneration.

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In age-related macular degeneration, oxidative damage and abnormal neovascularization in the retina are caused by the upregulation of vascular endothelium growth factor and reduced expression of Glutathione-S-transferase genes. Current treatments are only palliative. Compounds from cruciferous

Sulforaphane prevents dexamethasone-induced muscle atrophy via regulation of the Akt/Foxo1 axis in C2C12 myotubes.

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Muscle atrophy occurs in various catabolic conditions, including hormone imbalance, severe injury, sepsis, cancer, and aging. Dexamethasone (DEX) is a synthetic glucocorticoid and is used an anti-inflammatory agent. However, when chronically used, it is accompanied by side effects, such as, muscle

Progerin accumulation in nucleus pulposus cells impairs mitochondrial function and induces intervertebral disc degeneration and therapeutic effects of sulforaphane.

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Progerin, a truncated unprocessed lamin A protein, causes tissue aging and degeneration. In this study we explored the role of progerin in the pathogenesis of intervertebral disc degeneration (IDD). We also examined the effect of sulforaphane (SFN) on progerin accumulation and mitochondrial

Stereological survey of the ameliorative effects of sulforaphane and quercetin on renal tissue in unilateral ureteral obstruction in rats.

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Hydrostatic pressure, which is the result of urinary tract blockage, initiates renal injuries. The injuries are characterized by tubular dilatation and/or atrophy, tubular cell death, inflammatory process and progressive interstitial fibrosis with loss of renal parenchyma. The aim of this study was

Sulforaphane protects human chondrocytes against cell death induced by various stimuli.

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Chondrocyte cell death can contribute to cartilage degeneration in articular diseases, such as osteoarthritis (OA). Sulforaphane (SFN), a natural compound derived from cruciferous aliment, is well known as an anti-carcinogen, but according to recent evidence it also shows cytoprotective effects on a

Demonstration by redox fluorometry that sulforaphane protects retinal pigment epithelial cells against oxidative stress.

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OBJECTIVE To quantify the effects of oxidant challenge on the redox state of adult human retinal pigment epithelial cells using microscopic autofluorescence spectroscopy and to determine whether treatment with the isothiocyanate sulforaphane protects these cells against oxidative

Sulforaphane reduces the alterations induced by quinolinic acid: modulation of glutathione levels.

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Glutamate-induced excitotoxicity involves a state of acute oxidative stress, which is a crucial event during neuronal degeneration and is part of the physiopathology of neurodegenerative diseases. In this work, we evaluated the ability of sulforaphane (SULF), a natural dietary isothiocyanate, to

The Association Between Oxidative Stress Alleviation via Sulforaphane-Induced Nrf2-HO-1/NQO-1 Signaling Pathway Activation and Chronic Renal Allograft Dysfunction Improvement.

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OBJECTIVE Chronic renal allograft dysfunction (CRAD) is a leading cause of long-term renal allograft loss. Oxidative stress may account for the nonspecific interstitial fibrosis and tubular atrophy that occur in CRAD. An antioxidant intervention via Nrf2 signaling pathway activation might be a

Sulforaphane Attenuates Muscle Inflammation in Dystrophin-deficient mdx Mice via NF-E2-related Factor 2 (Nrf2)-mediated Inhibition of NF-κB Signaling Pathway.

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Inflammation is widely distributed in patients with Duchenne muscular dystrophy and ultimately leads to progressive deterioration of muscle function with chronic muscle damage, oxidative stress, and reduced oxidative capacity. NF-E2-related factor 2 (Nrf2) plays a critical role in defending against

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