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Tumor necrosis factor inhibition

Matthews, N., Neale, M.L., Jackson, S.K., and Stark, J.M., 1987, Tumor cell kilhng by tumor necrosis factor inhibition by anearobiotic condition, free-radical scavengers and inhibitors of arachidonate metabolism. Immunology 62 153-155 Miller, M.G., Rodgers, A., and Cohen, G.M., 1986, Mechanisms oftoxicity of naphthoquinones to isolated hepatocytes. Biochem. Pharmacol. 35 1177-1184 Minko, T., Kopeckova, P., and Kopecek, J., 1999, Comparison ofthe anticancer effect of free and HPMA copolymer-bound adtiamycin in human ovarian carcinoma cells. Pharmaceut. Res. 16 986-996... [Pg.168]

Tumor necrosis factor inhibition. Ethanol (95%) extract of the rhizome, in cell culture at a concentration of 100 pg/mL, was inactive on macrophage cell line RAW 264.7 vs EPS induction of TNF-az° zp Tumor promotion inhibition. Ethyl acetate and methanol extracts of the dried rhizome, in cell culture at a concentration of 50 pg/mL, produced weak activity on G3H/ lOTl/2 cells vs tetradecanoyl phorbol acetate-induced acetate phospholipid synthesis. The hexane extract was inactiveZ . Ethanol (95%) and petroleum ether extracts of the dried rhizome, in cell culture at a concentration of 160 and 80 pg/mL, re-... [Pg.542]

Sato, N., Fukuda, K., Nariuchi, H., and Sagara, N. Tumor necrosis factor inhibiting angiogenesis in vitro. JNCI, J. Nall. Cancer Inst. 79, 1383-1391 (1987). [Pg.81]

Hotamisligil, G.S., Murray, D.L., Choy, L.N., and Spiegelman, B.M. 1994. Tumor necrosis factor inhibits signaling from the insulin receptor. Proc. Natl. Acad. Sci. USA. 91 4854-4858. [Pg.93]

Sweiss NJ, Welsch MJ, Curran JJ, et al. Tumor necrosis factor inhibition as a novel treatment for refractory sarcoidosis. Arthritis Rheum 2005 53 788-791. [Pg.156]

Baughman RP. Tumor necrosis factor inhibition in treating sarcoidosis the American experience. Rev Port Pneumol 2007 13(suppl 2) S47-S50. [Pg.156]

Smith JR, Levinson RD, Holland GN, et al. Differential efficacy of tumor necrosis factor inhibition in the management of inflammatory eye disease and associated rheumatic disease. Arthritis Rheum 2001 45 252-257. [Pg.158]

Ahn SY, Cho CH, Park KG, Lee HI, Lee S, Park SK, Lee IK, Koh GY (2004) Tumor necrosis factor-alpha induces fractaUdne expression preferentially in arterial endothelial cells and mithramycin A suppresses TNF-alpha-induced fractaUdne expression. Am J Pathol 164 1663-1672 Alfano M, Schmidtmayerova H, Amelia CA, Pushkarsky T, Bukrinsky M (1999) The B-oligomer of pertussis toxin deactivates CC chemokine receptor 5 and blocks entry of M-tropic HIV-1 strains, [see comments]. J Exp Med 190 597-605 Ambrosini E, Alois F (2004) Chemokines and glial cells a complex network in the central nervous system. [Review] [239 refs]. Neurochem Res 29 1017-1038 Azuma Y, Ohura K (2002) Endomorphins 1 and 2 inhibit IL-10 and IL-12 production and innate immune functions, and potentiate NE-kappaB DNA binding in THP-1 differentiated to macrophagelike cells. Scand J Immunol 56 260-269... [Pg.332]

Chao CC, Molitor TW, Close K, Hu S, Peterson PK (1993) Morphine inhibits the release of tumor necrosis factor in human peripheral blood mononuclear cell cultures. Int J Immunopharmacol 15 447 53... [Pg.367]

Luo Y, Berman MA, Abromson-Leeman SR, Dorf ME (2003) Tumor necrosis factor is required for RANTES-induced astrocyte monocyte chemoattractant protein-1 production. Glia 43 119-127 Machelska H, Stein C (2006) Leukocyte-derived opioid peptides and inhibition of pain. J Neuroimmune Pharmacol 1 90-97... [Pg.372]

Selective inhibition of tumor necrosis factor-induced vascular cell adhesion molecule-1 gene expression by a novel flavonoid. Lack of effect on trascriptional factor NF-kB Arteriosclerosis, Thrombosis and Vascular Biology 16, 1501-8. [Pg.16]

A2. Aderka, D., Le, J., and Vilcek, J., IL-6 inhibits lipopolysaccharide-induced tumor necrosis factor production in cultured human monocytes U937 cells, and in mice. J. Immunol. 143, 3517-352) (1989). [Pg.107]

D19. Dinarello, C. A., Okusawa, S., and Gelfland, J. A., Interleukin-1 induces a shock-like state in rabbits Synergism with tumor necrosis factor and the effect of cyclooxygenase inhibition. In Molecular and Cellular Mechanisms of Septic Shock. Alan R. Liss, New York, 243-263... [Pg.113]

Jl. Jaattela, M., Overexpression of major heat shock protein HSP70 inhibits tumor necrosis factor-induced activation of phospholipase A2. J. Immunol. 151,4286-4294 (1993). [Pg.118]

K9. Kilboum, R. G., Gross, S. S., Jubran, A., Adams, J., Griffith, O. W., Levi, R., and Lodato, R. F., A,c -Methyl-L-arginine inhibits tumor necrosis factor-induced hypotension. Proc. Natl. Acad. Sci. USA. 87, 3629-3632 (1990). [Pg.119]

P16. van der Poll, T., Coyle, S. M., Barbosa, K., Braxton, C. C., and Lowry, S. F., Epinephrine inhibits tumor necrosis factor-alpha and potentiates interleukin-10 production during human en-dotoxemia. J. Clin. Invest. 97,713-719 (1996). [Pg.125]

The ability of natural products to inhibition of topoisomerase and precipitate apoptosis mentioned in this chapter are two abilities among several others, of which inhibition of microtubule formation, inhibition of DNA polymerase, protein kinases, protein phosphatase and aromatase, and the use of cytokines, interleukins, and tumor necrosis factor and yet uncovered cellular targets. [Pg.222]

Flieger, D., G. Reithmuller, and H.W.L. Ziegler-Heitbrock. 1989. Zn inhibits both tumor necrosis factor-mediated DNA fragmentation and cytolysis. Inter. Jour. Cancer 44 315-319. [Pg.731]

The major types of drug therapy used in IBD include aminosalicylates, glucocorticoids, immunosuppressive agents (azathioprine, mercaptopu-rine, cyclosporine, and methotrexate), antimicrobials (metronidazole and ciprofloxacin), and agents to inhibit tumor necrosis factor-a (TNF-a) (anti-TNF-a antibodies). [Pg.299]

Tumor necrosis factor a (TNF-a) is a multifunctional cytokine produced by activated monocytes-macrophages. TNF-a is one of the most potent osteoclastogenic cytokines produced in inflammation, and, in addition, TNF-a induces IL-1 synthesis. Like the other known stimulators of bone resorption, it acts through osteoblastic cells however, it has been demonstrated that TNF-a is able to induce osteoclast formation from stromal-depleted macrophages, with potency similar to that of RANKL (Kobayashi et al. 2000). TNF-a is able to induce bone resorption in vitro (Thomson et al. 1987) as well as in vivo (Koning et al. 1988). Osteoclasts induced by TNF-a have the capacity to form resorption pits on dentine slices only in the presence of IL-la. TNF-a, together with IL-1, plays an important role in bone resorption in inflammatory diseases (Kobayashi et al. 2000). Inhibition of TNF by TNF binding protein (TNFbp) completely prevents bone loss and osteoclast formation (Kimble et al. 1997). [Pg.176]

Kwon BS, Wang S, Udagawa N, Haridas V, Lee ZH, Kim KK, Oh KO, Greene J, Li Y, Su J, Gentz R, Aggarwal BB, Ni J (1998) TR1, a new member of the tumor necrosis factor receptor superfamily, induces fibroblast proliferation and inhibits osteoclastogenesis and bone resorption. FASEB J 12 845-854... [Pg.190]


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See also in sourсe #XX -- [ Pg.195 ]




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