Inhibition of glucocorticoid-induced changes of Na+, K+-ATPase in rat lens by a glucocorticoid receptor antagonist RU486

Xie, Guoli; Zhang, Pengcheng; Lu, Zifan

doi:10.1016/j.exer.2010.07.005

Cited by 7 publications

(7 citation statements)

References 64 publications

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“…Among them, Vim (vimentin) encoding a protein involved in structural maintenance, was down-regulated in most treatments, but up-regulated by ischemic lesion. GR-mediated signaling reduces Vim expression, which is possibly linked to visual function [66] and astrocyte morphology [67]. Increased VIM expression was observed in the post-ischemic kidney [68], which confirms the present findings.…”

Section: Discussionsupporting

confidence: 89%

Lifetime Stress Cumulatively Programs Brain Transcriptome and Impedes Stroke Recovery: Benefit of Sensory Stimulation

et al. 2014

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Prenatal stress (PS) represents a critical variable affecting lifetime health trajectories, metabolic and vascular functions. Beneficial experiences may attenuate the effects of PS and its programming of health outcomes in later life. Here we investigated in a rat model (1) if PS modulates recovery following cortical ischemia in adulthood; (2) if a second hit by adult stress (AS) exaggerates stress responses and ischemic damage; and (3) if tactile stimulation (TS) attenuates the cumulative effects of PS and AS. Prenatally stressed and non-stressed adult male rats underwent focal ischemic motor cortex lesion and were tested in skilled reaching and skilled walking tasks. Two groups of rats experienced recurrent restraint stress in adulthood and one of these groups also underwent daily TS therapy. Animals that experienced both PS and AS displayed the most severe motor disabilities after lesion. By contrast, TS promoted recovery from ischemic lesion and reduced hypothalamic-pituitary-adrenal axis activity. The data also showed that cumulative effects of adverse and beneficial lifespan experiences interact with disease outcomes and brain plasticity through the modulation of gene expression. Microarray analysis of the lesion motor cortex revealed that cumulative PS and AS interact with genes related to growth factors and transcription factors, which were not affected by PS or lesion alone. TS in PS+AS animals reverted these changes, suggesting a critical role for these factors in activity-dependent motor cortical reorganization after ischemic lesion. These findings suggest that beneficial experience later in life can moderate adverse consequences of early programming to improve cerebrovascular health.

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Section: Discussionsupporting

confidence: 89%

Lifetime Stress Cumulatively Programs Brain Transcriptome and Impedes Stroke Recovery: Benefit of Sensory Stimulation

et al. 2014

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“…The homeostasis of these ions is crucial in the processes of cell cycle regulation, cell proliferation, and apoptosis. On the other hand, some hormones are able to affect processes closely connected with the activity and conformation of Na + /K + -ATPase [119], e.g., aldosterone [120], thyroid hormones [119,121], glucocorticoids [122], catecholamines [123], and insulin [124]. But cAMP [125] also affects the expression of Na + /K + -ATPase in different tissues.…”

Section: Introductionmentioning

confidence: 99%

From Na+/K+-ATPase and Cardiac Glycosides to Cytotoxicity and Cancer Treatment

Babula¹,

Masařík²,

Adam³

et al. 2013

ACAMC

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The cardiac glycosides are a group of compounds isolated from plants and some animals. They have been used in therapy for heart failure for many years. The cytotoxic effect of many cardiac glycosides has been demonstrated, but the mechanism of action is very complicated and complex, and Na+/K+-ATPase surely plays a crucial role in it. On the other hand, Na+/K+-ATPase is regulated by many endogenous factors, such as hormones or FXYD proteins, whose role in regulating the cell cycle has been studied intensively. This review focuses on the role of Na+/K+-ATPase in regulating the cell growth, the cell cycle and the cell proliferation and on the involvement of cardiac glycosides in regulating Na+/K+-ATPase. The cytotoxic effect of cardiac glycosides is discussed with respect to the apoptotic mechanisms possibly induced by these compounds. Novel strategies in cancer therapy based on cardiac glycosides are discussed as are possibilities for counteracting multidrug resistance by using cardiac glycosides. The aim of this review is to present cardiac glycosides not only as pharmaceuticals used in the management of heart failure, but also as potent cytotoxic agents with potential uses in cancer treatment.

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“…For rat lens culture, eyes from 21-dayold Sprague-Dawley male rats were enucleated to expel the lens using plastic-coated forceps and fine scissors. Eyes were immediately transferred to Dulbecco's MEM (pH 7.2; Sigma, St. Louis, MO), containing 0.1% bovine serum albumin (BSA; GibcoBRL, Grand Island, NY) and antibiotic solution (GibcoBRL; 100 U/mL penicillin, 100 µg/mL streptomycin, and 0.25 µg/mL amphotericin B) [52]. The culture media was changed daily.…”

Section: Ex Vivo Rat Lens Culture and Drug Treatmentmentioning

confidence: 99%

N-acetylcysteine amide protects against dexamethasone-induced cataract related changes in cultured rat lenses

Tobwala¹,

Pınarcı²,

Maddirala³

et al. 2014

ABC

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Glucocorticoids (GCs) are one of the most widely used immunosuppressive and anti-inflammatory agents. However, their long term and systemic use is associated with adverse drug reactions including posterior subcapsular cataracts as one of its ocular complications. Balanced redox state is crucial for maintenance of lens transparency, and a high content of glutathione (GSH) in the lens is believed to play a key role in doing so. Depletion of GSH is implicated in the etiopathogenesis of dexamethasone-induced cataracts and, therefore, the present study was sought to evaluate the efficacy of a novel thiol antioxidant, N-acetylcysteine amide (NACA), in preventing dexamethasone-induced cataractogenesis. Cataract formation was induced by incubation of rat lenses with 5 µM dexamethasone. To assess whether NACA had a significant impact on dexamethasone-induced cataracts, the rat lenses were divided into four groups: 1) control group (Dulbecco's Modified Eagle Medium (DMEM), 2) dexamethasone group (DMEM with 5 µM dexamethasone), 3) NACA-only group (50 µM NACA solution), and 4) NACA pretreatment group (50 µM NACA for 6 hours followed by 5 µM dexamethasone only for 18 hours). Lenses were cultured for 7 days at 37˚C under 5% CO 2 . Lenses were evaluated daily using a dissecting microscope and photographed and graded for the development of opacity. The rat lenses in both the control and the NACA-only groups were clear, whereas all lenses within the dexamethasone-only group developed well-defined cataracts. Overall observations indicated that NACA inhibits cataract formation by limiting lipid peroxidation and increasing the ratio of GSH/GSSG in lens. Therefore, NACA can be developed into a potential adjunctive therapeutic option for patients undergoing therapy with GCs to inhibit glucocorticoid-induced cataracts.

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Inhibition of glucocorticoid-induced changes of Na+, K+-ATPase in rat lens by a glucocorticoid receptor antagonist RU486

Cited by 7 publications

References 64 publications

Lifetime Stress Cumulatively Programs Brain Transcriptome and Impedes Stroke Recovery: Benefit of Sensory Stimulation

Lifetime Stress Cumulatively Programs Brain Transcriptome and Impedes Stroke Recovery: Benefit of Sensory Stimulation

From Na+/K+-ATPase and Cardiac Glycosides to Cytotoxicity and Cancer Treatment

N-acetylcysteine amide protects against dexamethasone-induced cataract related changes in cultured rat lenses

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