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Nutrition: Zinc

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Total 98 results found since Jan 2013.

Molecular screening and analysis of novel therapeutic inhibitors against c-Jun N-terminal kinase
Abstractc-Jun N-terminal kinase is an important regulator, activating several transcription factors in response to proinflammatory cytokines, ultraviolet radiations, environmental stress, hypoxia and osmotic shock and is known to be reported a cause for many diseases, such as diabetes, cancer, inflammation, stroke, etc. In the present study, we aim to predict novel therapeutic leads against c-Jun N-terminal kinase-3 by employing structure based virtual screening in combination with various in silico toxicity filters. We screened ZINC database virtually using a known potent c-Jun N-terminal kinase inhibitor, SP600125, as re...
Source: Medicinal Chemistry Research - July 29, 2017 Category: Chemistry Source Type: research

MicroRNAs Mediated MMP Regulation: Current Diagnostic and Therapeutic Strategies for Metabolic Syndrome.
Abstract Metabolic syndrome (MS) is a global socioeconomic problem rapidly progressing in accordance with increasing body mass index (BMI) and age. It is a consortium of risk factors, such as dyslipidaemia, insulin resistance, leptin resistance, reduced adiponectin, glucose intolerance, hyperglycemia, and hypertension. Collectively, these factors accelerate the onset of type 2 diabetes mellitus, cardiovascular disease, stroke, and certain cancers such as breast, liver pancreatic, and colon cancer. Extracellular matrix (ECM) and basement membrane remodeling play a central role during pathogenesis of MS as they regu...
Source: Current Gene Therapy - July 7, 2017 Category: Genetics & Stem Cells Authors: Saxena S, Jain A, Rani V Tags: Curr Gene Ther Source Type: research

Reduction of zinc accumulation in mitochondria contributes to decreased cerebral ischemic injury by normobaric hyperoxia treatment in an experimental stroke model.
In this study, we investigate whether NBO could regulate zinc accumulation in the penumbra and prevent mitochondrial damage in penumbral tissue using a transient cerebral ischemic rat model. Our results showed that NBO significantly reduced zinc staining positive cells and zinc-staining intensity in penumbral tissues, but not in the ischemic core. Moreover, ischemia-induced zinc accumulation in mitochondria, isolated from penumbral tissues, was greatly attenuated by NBO or a zinc specific chelator, N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN). NBO or TPEN administration stabilized the mitochondrial membrane po...
Source: Experimental Neurology - April 16, 2015 Category: Neurology Authors: Dong W, Qi Z, Liang J, Shi W, Zhao Y, Luo Y, Ji X, Liu KJ Tags: Exp Neurol Source Type: research

Autophagy Mediates Astrocyte Death During Zinc-Potentiated Ischemia-Reperfusion Injury.
Abstract Pathological release of excess zinc ions and the resultant increase in intracellular zinc has been implicated in ischemic brain cell death, although the underlying mechanisms are not fully understood. Since zinc promotes the formation of the autophagic signal, reactive oxygen species (ROS), and increases autophagy, a known mechanism of cell death, we hypothesized that autophagy is involved in zinc-induced hypoxic cell death. To study this hypothesis, we determined the effect of zinc on autophagy and ROS generation in C8-D1A astrocytes subjected to hypoxia and rexoygenation (H/R), simulating ischemic strok...
Source: Biological Trace Element Research - March 12, 2015 Category: Biology Authors: Pan R, Timmins GS, Liu W, Liu KJ Tags: Biol Trace Elem Res Source Type: research

Zinc: indications in brain disorders
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Source: Fundamental and Clinical Pharmacology - February 1, 2015 Category: Drugs & Pharmacology Authors: Atish Prakash, Kanchan Bharti, Abu Bakar Abdul Majeed Tags: Review Article Source Type: research

Indomethacin preconditioning induces ischemic tolerance by modifying zinc availability in the brain.
This study found that chronic pretreatment of rats with indomethacin, a non-selective cyclooxygenase inhibitor, provided tolerance to ischemic injuries in an animal model of stroke by eliciting moderate zinc elevation in neurons. Consecutive intraperitoneal injection of indomethacin (3mg/kg/day for 28days) led to modest increases in intraneuronal zinc as well as synaptic zinc content, with no significant stimulation of neuronal death. Furthermore, indomethacin induced the expression levels of intracellular zinc homeostatic and neuroprotective proteins, rendering the brain resistant against ischemic damages and improving ne...
Source: Neurobiology of Disease - January 3, 2015 Category: Neurology Authors: Lee J, Oh SB, Hwang J, Suh N, Jo D, Kim JS, Koh J Tags: Neurobiol Dis Source Type: research

Chelating Intracellularly Accumulated Zinc Decreased Ischemic Brain Injury Through Reducing Neuronal Apoptotic Death Basic Sciences
Conclusions— Ischemia-induced high accumulation of intracellular zinc significantly contributed to ischemic brain damage through promotion of neuronal apoptotic death. Removing zinc may be an effective and novel approach to reduce ischemic brain injury.
Source: Stroke - March 24, 2014 Category: Neurology Authors: Zhao, Y., Pan, R., Li, S., Luo, Y., Yan, F., Yin, J., Qi, Z., Yan, Y., Ji, X., Liu, K. J. Tags: Acute Cerebral Infarction Basic Sciences Source Type: research

Zinc Promotes the Death of Hypoxic Astrocytes by Upregulating Hypoxia-Induced Hypoxia-Inducible Factor-1alpha Expression via Poly(ADP-ribose) Polymerase-1.
CONCLUSIONS: Our studies show that zinc promotes hypoxic cell death through overexpression of the hypoxia response factor HIF-1α via the cell fate determine factor PARP-1 modification, which provides a novel mechanism for zinc-mediated ischemic brain injury. PMID: 23582235 [PubMed - as supplied by publisher]
Source: CNS Neuroscience and Therapeutics - April 13, 2013 Category: Neuroscience Authors: Pan R, Chen C, Liu WL, Liu KJ Tags: CNS Neurosci Ther Source Type: research