l leucine/نخر

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Tumor necrosis factor-alpha mediates inhibitory effect of lipopolysaccharide on L-leucine intestinal uptake.

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Tumor necrosis factor-alpha (TNF-alpha) has been proposed as an early proximal mediator of many metabolic and physiologic responses during septic shock. We have previously shown that direct addition to tissue (local effect) or intravenous administration (systemic effect) of lipopolysaccharide (LPS)

Involvement of a serine protease in tumour-necrosis-factor-mediated cytotoxicity.

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We investigated the effect of various protease inhibitors on the anti-proliferative and cytotoxic action of tumour necrosis factor (TNF) on mouse L929 fibrosarcoma cells. 1. The following serine-type protease inhibitors led to inhibition of TNF action: phenylmethylsulfonyl fluoride, N

Inhibition of L-leucine methyl ester mediated killing of THP-1, a human monocytic cell line, by a new anti-inflammatory drug, T614.

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T614 (3-formylamino-7-methylsulfonylamino-6-phenoxy-4H-1-benzopyran-4-o ne) is a member of the family of methanesulfonanilide non-steroidal anti-inflammatory drugs (mNSAIDs), most of which act as cyclooxygenase (COX)-2 inhibitors. L-leucine methyl ester (Leu-OME) is a reagent which has been shown to

Synthesis of caged compounds of L-leucyl-L-leucine methyl ester, an apoptosis inducer, and their cytotoxic activity.

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In this study, we newly synthesized caged compounds of L-leucyl-L-leucine methyl ester and examined their photochemical and immunological properties. From the viewpoints of solubility in phosphate-buffered saline containing 1% dimethyl sulfoxide as well as photoreactivity, we chose two caged

Modulation of RIP1 ubiquitylation and distribution by MeBS to sensitize cancer cells to tumor necrosis factor α-induced apoptosis.

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Overexpression of anti-apoptosis protein cIAP1 due to its genetic amplification is found in certain cancers such as esophageal squamous cell carcinoma, hepatocellular carcinoma, cervical cancer and lung cancer, and plays a significant role in resistance to cancer therapy. We previously reported that

Synthesis, photoreactivity and cytotoxic activity of caged compounds of L-leucyl-L-leucine methyl ester, an apoptosis inducer.

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L-Leucyl-L-leucine methyl ester (Leu-Leu-OMe), an apoptosis inducer in natural killer cells and macrophages, was caged with trans-o-hydroxycinnamoyl (3a-d), trans-o-mercaptocinnamoyl (4) and o-nitrobenzyl derivatives (5a, b), and the photochemical reactivity of these derivatives in

Small duct cholangitis induced by N-formyl L-methionine L-leucine L-tyrosine in rats.

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Primary sclerosing cholangitis (PSC) frequently accompanies inflammatory bowel diseases. In an attempt to increase our understanding of the pathogenesis of PSC, we studied bile duct changes in rats with colitis which had been given N-formyl L-methionine L-leucine L-tyrosine (fMLT) rectally; fMLT is

Tumor necrosis factor alpha stimulates taurine uptake and transporter gene expression in human intestinal Caco-2 cells.

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The effect of cytokines on the taurine uptake by human intestinal epithelial Caco-2 cells was investigated. Among the various cytokines tested, tumor necrosis factor alpha (TNF-alpha) markedly increased the taurine uptake by Caco-2 cells, resulting in an increase in the intracellular taurine level.

Inhibitory effect of TNF-alpha on the intestinal absorption of galactose.

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Sepsis is a systemic response to infection in which toxins, such as bacterial lipopolysaccharide (LPS), stimulate the production of inflammatory mediators like the cytokine tumor necrosis factor alpha (TNF-alpha). Previous studies from our laboratory have revealed that LPS inhibits the intestinal

Role of S-nitrosothiol transport in the cardioprotective effects of S-nitrosocysteine in rat hearts.

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The objective of this study was to determine if prior exposure of rat hearts to S-nitrosocysteine (CysNO) was able to provide protection against reperfusion injury. We probed NO release using the extracellular NO scavenger oxyhemoglobin (oxyHb), and we examined the involvement of the amino acid

Enhanced susceptibility of cis-diamminedichloroplatinum-treated K562 cells to lysis by peripheral blood lymphocytes and lymphokine activated killer cells.

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BACKGROUND Previous studies have reported that cis-diamminedichloroplatinum (II) (CDDP) exhibits various immunomodulating activities. The current study investigates the effect of CDDP on the susceptibility of K562 cells to lysis by peripheral blood lymphocytes (PBL), natural killer (NK) cells, and

Functional and morphological changes of the exocrine pancreas in ciclosporin-treated rats.

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We have examined whether or not ciclosporin A (CsA) affects structure and function of the exocrine pancreas. Male Wistar rats were treated once a day for 7 days with intraperitoneal injections of vehicle or 5, 15, 30, or 50 mg/kg of CsA. Following the CsA treatment, incorporations of [3H]thymidine

Effect of lead acetate on nitrite production by murine brain endothelial cell cultures.

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One of the mechanisms by which lead may cause a perturbation in the nervous system is the alteration of endothelial cell function. This study investigated the effect of lead acetate on constitutive and cytokine-induced production of nitrite, a marker of nitric oxide, in brain microvascular

Antigen presentation by Leishmania mexicana-infected macrophages: activation of helper T cells specific for amastigote cysteine proteinases requires intracellular killing of the parasites.

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Leishmania mexicana amastigotes proliferate in the phagolysosomes of mammalian macrophages. The parasites abundantly synthesize lysosomal cysteine proteinases, which are encoded by the lmcpb gene family. One of these genes was overexpressed in Escherichia coli, and the purified recombinant protein

Neutrophil adhesion inhibition prolongs survival of cardiac allografts with hyperacute rejection.

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Hyperacute rejection results in rapid destruction of a cardiac allograft and is characterized by infiltration of neutrophils into the donor organ. We sought to ameliorate this response by using a potent inhibitor of neutrophil adhesion to vascular endothelium, NPC 15669

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