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Inhibition by N-acetyl-L-cysteine of interleukin-6 mRNA induction and activation of NF kappa B by tumor necrosis factor alpha in a mouse fibroblastic cell line, Balb/3T3.

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Redox-based modulation plays a role in transcriptional control of gene expression. In the present study, we investigated the possible role of reactive oxygen species in the induction of interleukin-6 (IL-6) mRNA and in increases in NF kappa B binding activity by tumor necrosis factor (TNF) alpha

N-acetyl-L-cysteine protects endothelial cells but not L929 tumor cells from tumor necrosis factor-alpha-mediated cytotoxicity.

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The effect of N-acetyl-L-cysteine on the cytotoxicity of tumor necrosis factor-alpha was investigated in cultured bovine pulmonary artery endothelial cells and L929 mouse tumor cells. In endothelial cells, a 72-h incubation with tumor necrosis factor-alpha (100 ng/ml) reduced the number of viable

N-acetyl-L-cysteine exhibits antitumoral activity by increasing tumor necrosis factor alpha-dependent T-cell cytotoxicity.

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Because of its anticarcinogenic and antimutagenic properties, N-acetyl-L-cysteine (NAC) has been proposed for cancer treatment. Here we present a mechanism of action for NAC in cancer. Our data show that NAC (1) induces an early and sustained increase of membrane tumor necrosis factor alpha (TNF

Azathioprine acts upon rat hepatocyte mitochondria and stress-activated protein kinases leading to necrosis: protective role of N-acetyl-L-cysteine.

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Azathioprine is an immunosuppressant drug widely used. Our purpose was to 1) determine whether its associated hepatotoxicity could be attributable to the induction of a necrotic or apoptotic effect in hepatocytes, and 2) elucidate the mechanism involved. To evaluate cellular responses to

Regulation of apoptosis/necrosis execution in cadmium-treated human promonocytic cells under different forms of oxidative stress.

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Pulse-treatment of U-937 human promonocytic cells with cadmium chloride followed by recovery caused caspase-9/caspase-3-dependent, caspase-8-independent apoptosis. However, pre-incubation with the glutathione (GSH)-suppressing agent DL-buthionine-(S,R)-sulfoximine (cadmium/BSO), or co-treatment with

Sulfur-containing amino acids that increase renal glutathione protect the kidney against papillary necrosis induced by 2-bromoethylamine.

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Papillary necrosis was observed in the kidneys of rats, 72 h after receiving a single injection of bromoethylamine (BEA). This effect was associated with renal glutathione (GSH) depletion 1 h after the administration of BEA. Stimulation of renal GSH synthesis by pretreatment of the animals either

Oxidative stress induction by (+)-cordiaquinone J triggers both mitochondria-dependent apoptosis and necrosis in leukemia cells.

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(+)-Cordiaquinone J is a 1,4-naphthoquinone isolated from the roots of Cordia leucocephala that has antifungal and larvicidal effects. However, the cytotoxic effects of (+)-cordiaquinone J have never being explored. In the present study, the effect of (+)-cordiaquinone J on tumor cells viability was

Antioxidants differentially regulate activation of nuclear factor-kappa B, activator protein-1, c-jun amino-terminal kinases, and apoptosis induced by tumor necrosis factor: evidence that JNK and NF-kappa B activation are not linked to apoptosis.

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Tumor necrosis factor (TNF) is known to mediate its signaling through generation of reactive oxygen species (ROS), but the type of TNF signal regulated by ROS and the nature of the ROS species involved are not fully understood. In this report, we investigated the effect of various superoxide radical

Protective effects of N-acetyl-L-cysteine in endotoxemia.

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Because oxygen free radicals have been implicated in the endothelial cell damage and in the myocardial depression occurring during severe sepsis, we investigated whether N-acetyl-L-cysteine (NAC) could influence the oxygen extraction capabilities during an acute reduction in blood flow induced by

Activation of transcriptionally active nuclear factor-kappaB by tumor necrosis factor-alpha and its inhibition by antioxidants in rat thyroid FRTL-5 cells.

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ABSTRACT Tumor necrosis factor-alpha (TNF-alpha) exerts pleiotropic effects on thyroid follicular cells. However, the intracellular signaling pathway for the TNF-alpha action has not been well elucidated. The present study examined the effects of TNF-alpha on the activation of nuclear factor-kappa B

Oxidative stress signalling: a potential mediator of tumour necrosis factor alpha-induced genomic instability in primary vascular endothelial cells.

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Studying the potential role of tumour necrosis factor (TNF)alpha in the initiation of genomic instability is necessary to understand whether TNFalpha can serve as a signalling mediator of radiation-induced genomic instability in non-irradiated bystander cells. In this study, we examined whether

Rucaparip (Rubraca ^®) induces necrosis via upregulating the expression of RIP1 and RIP3 in ovarian cancer cells

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In the current study we investigated the inhibitory effect of rucaparib (Rubraca^®) on human ovarian cancer SKOV3 and A2780 cells and its possible mechanism. Cancer cells and human normal ovarian epithelial IOSE80 cells were treated with Rubraca^® at different concentrations.

Hydrogen peroxide and tumour necrosis factor-alpha induce NF-kappaB-DNA binding in primary human T lymphocytes in addition to T cell lines.

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Reactive oxygen intermediates (ROIs), such as hydrogen peroxide (H2O2), have been implicated as second messengers in the activation of NF-kappaB by a variety of stimuli, including tumour necrosis factor-alpha (TNF-alpha). The aim of the present study was to examine the effects of ROIs on NF-kappaB

Role of early- or late-phase activation of p38 mitogen-activated protein kinase induced by tumour necrosis factor-alpha or 2,4-dinitrochlorobenzene during maturation of murine dendritic cells.

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Dendritic cells (DCs) are maturated by a variety of stimuli. However, the precise mechanisms underlying the maturation of DCs are not fully understood. In the present study, we analysed the effects of tumour necrosis factor-alpha (TNF-alpha) and 2,4-dinitrochlorobenzene (DNCB) on phenotypic

[Protective effect of N-acetyl-L-cysteine on liver and lung injury in mice after partial hepatic ischemia/reperfusion].

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OBJECTIVE To investigate the changes in Toll-like receptor 2/4(TLR2/4) gene expression in liver and lung in ischemia/reperfusion (I/R) injury with or without preconditioning of N-acetyl-L-cysteine (NAC). METHODS BALB/c mice were used in a model of partial hepatic I/R injury and randomly divided into

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n acetyl l cysteine/نخر

Inhibition by N-acetyl-L-cysteine of interleukin-6 mRNA induction and activation of NF kappa B by tumor necrosis factor alpha in a mouse fibroblastic cell line, Balb/3T3.

N-acetyl-L-cysteine protects endothelial cells but not L929 tumor cells from tumor necrosis factor-alpha-mediated cytotoxicity.

N-acetyl-L-cysteine exhibits antitumoral activity by increasing tumor necrosis factor alpha-dependent T-cell cytotoxicity.

Azathioprine acts upon rat hepatocyte mitochondria and stress-activated protein kinases leading to necrosis: protective role of N-acetyl-L-cysteine.

Regulation of apoptosis/necrosis execution in cadmium-treated human promonocytic cells under different forms of oxidative stress.

Sulfur-containing amino acids that increase renal glutathione protect the kidney against papillary necrosis induced by 2-bromoethylamine.

Oxidative stress induction by (+)-cordiaquinone J triggers both mitochondria-dependent apoptosis and necrosis in leukemia cells.

Antioxidants differentially regulate activation of nuclear factor-kappa B, activator protein-1, c-jun amino-terminal kinases, and apoptosis induced by tumor necrosis factor: evidence that JNK and NF-kappa B activation are not linked to apoptosis.

Protective effects of N-acetyl-L-cysteine in endotoxemia.

Activation of transcriptionally active nuclear factor-kappaB by tumor necrosis factor-alpha and its inhibition by antioxidants in rat thyroid FRTL-5 cells.

Oxidative stress signalling: a potential mediator of tumour necrosis factor alpha-induced genomic instability in primary vascular endothelial cells.

Rucaparip (Rubraca ®) induces necrosis via upregulating the expression of RIP1 and RIP3 in ovarian cancer cells

Hydrogen peroxide and tumour necrosis factor-alpha induce NF-kappaB-DNA binding in primary human T lymphocytes in addition to T cell lines.

Role of early- or late-phase activation of p38 mitogen-activated protein kinase induced by tumour necrosis factor-alpha or 2,4-dinitrochlorobenzene during maturation of murine dendritic cells.

[Protective effect of N-acetyl-L-cysteine on liver and lung injury in mice after partial hepatic ischemia/reperfusion].

قاعدة بيانات الأعشاب الطبية الأكثر اكتمالا التي يدعمها العلم

Rucaparip (Rubraca ^®) induces necrosis via upregulating the expression of RIP1 and RIP3 in ovarian cancer cells