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Interleukin-1 induction of aggrecanase gene expression in human articular chondrocytes is mediated by mitogen-activated protein kinases.

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OBJECTIVE We investigated the unknown molecular mechanisms of Interleukin-1 (IL-1β)-induced cartilage aggrecan degeneration by aggrecanase (ADAMTS-A Disintegrin And Metalloproteinase with ThromboSpondin motifs) in human articular chondrocytes, a model mimicking human arthritis. METHODS Chondrocytes

Nitric oxide triggers the toxicity due to glutathione depletion in midbrain cultures through 12-lipoxygenase.

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Glutathione (GSH) depletion is the earliest biochemical alteration shown to date in brains of Parkinson's disease patients. However, data from animal models show that GSH depletion by itself is not sufficient to induce nigral degeneration. We have previously shown that non-toxic inhibition of GSH

Glial cells mediate toxicity in glutathione-depleted mesencephalic cultures.

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We have examined the role of glial cells in the toxicity that results from inhibition of reduced glutathione (GSH) synthesis by L-buthionine sulfoximine (BSO) in mesencephalic cell cultures. We show that GSH depletion, to levels that cause total cell loss in cultures containing neurons and glial

Ageing of Neurospora crassa. I. Evidence for the free radical theory of ageing from studies of a natural-death mutant.

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A recessive mutant of Neurospora crassa, called natural-death, is characterized by a decreasing clonal growth potential under all nutritional conditions and the irreversible cessation of growth. The primary molecular defect of this mutant is not known. Evidence presented here, based upon

Ageing of Neurospora crassa. VII. Accumulation of fluorescent pigment (lipofuscin) and inhibition of the accumulation by nordihydroguairetic acid.

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Continuous administration of the antioxidant nordihydroguairetic acid to clones of the natural-death nutant or wild-type Neurospora crassa growing on 5-fluorotryptophan not only alleviates the time-dependent deterioration of growth rate (senescence), but also inhibits the accumulation of a

Ageing of Neurospora crassa. III. Induction of cellular death and clonal senescence of an inositol-less mutant by inositol starvation and the protective effect of dietary antioxidants.

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Clonal growth rate and cellular viability of an inositol-less mutant of Neurospora crassa decline rapidly during deprivation of dietary inositol. Dietary antioxidants, either nordihydroguaiaretic acid, vitamin E or 3,5-ditert.-butyl-4-hydroxybenzyl alcohol, protected cells and clones of the mutant

Studies on the mechanisms causing inhibition of insulin secretion in rat pancreatic islets exposed to human interleukin-1 beta indicate a perturbation in the mitochondrial function.

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This study aimed at a more detailed characterization of the mechanisms by which interleukin 1 (IL-1) inhibits insulin secretion. For this purpose, isolated rat pancreatic islets were kept in tissue culture for 5 days in medium RPMI 1640 plus 10% calf serum. The islets were subsequently transferred

Virtual screening for functional foods against the main protease of SARS-CoV-2

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The special attention was paid on the interaction between functional foods and the main protease of severe acute respiratory syndrome coronavirus (SARS-CoV-2). Here, 10,870 ligands were employed and screened by the molecular docking, which involved 12 kinds of functional foods (carbohydrates, fatty

Calcium influx inhibition by steroids and analogs in C2C12 skeletal muscle cells.

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Glucocorticoids, namely alpha-methylprednisolone (PDN) and deflazacort, are the only drugs reported to have a beneficial effect on the degenerative course of Duchenne muscular dystrophy (DMD). Increased cytosolic calcium concentrations ([Ca2+]c) have been implicated as one of the pathological events

Identification of polyphenolic compounds and black tea extract as potent inhibitors of lipid membrane destabilization by Aβ₄₂ aggregates.

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Amyloid-β (Aβ) aggregation is a recognized key process in the pathogenesis of Alzheimer's disease (AD). Misfolded Aβ peptides self-assemble into higher-order oligomers that compromise membrane integrity, leading to synaptic degeneration and neuronal cell death. The main aim of this study was to

Antioxidant compounds have potent anti-fibrillogenic and fibril-destabilizing effects for alpha-synuclein fibrils in vitro.

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The aggregation of alpha-synuclein (alphaS) in the brain has been implicated as a critical step in the development of Lewy body diseases (LBD) and multiple system atrophy (MSA). Various antioxidants not only inhibit the formation of beta-amyloid fibrils (fAbeta), but also destabilize preformed fAb

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