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ALOX5 — TNF

Text-mined interactions from Literome

Anthonsen et al., J Biol Chem 2001 : We show that in addition to inhibitors of secretory and cytosolic PLA(2)s, 5-lipoxygenase inhibitors attenuate TNF-alpha- and IL-1beta stimulated NF-kappaB activation
Bertolini et al., Pharmacol Res 2001 : Moreover, inhibition of 5-lipoxygenase indirectly reduces the expression of TNF-alpha ( a cytokine that plays a key role in inflammation )
Bertolini et al., Curr Med Chem 2002 (Gastrointestinal Diseases...) : The products generated by the 5-lipoxygenase pathway ( leukotrienes ) are particularly important in inflammation : indeed, leukotrienes increase microvascular permeability and are potent chemotactic agents ; moreover, inhibition of 5-lipoxygenase indirectly reduces the expression of TNF-alpha ( a cytokine that plays a key role in inflammation )
Ogata et al., Infect Immun 1992 : This study was performed to examine the effects of a 5-lipoxygenase inhibitor ( AA-861 ), a selective leukotriene receptor antagonist ( ONO-1078 ), and a cyclooxygenase inhibitor ( indomethacin ) on endotoxin induced mortality and TNF production in mice
Vanags et al., Cell Death Differ 1997 : However, the mechanisms by which these inhibitors act, remain unexplained since there was no 5-LO expression in the U937 cells and no AA release followed their stimulation with TNF plus CHX
Ferrándiz et al., Agents Actions 1991 (Disease Models, Animal...) : In vitro studies have demonstrated that 5-lipoxygenase products promote the production of TNF by activated macrophages, suggesting that 5-lipoxygenase inhibitors may have therapeutic utility for the treatment of inflammatory conditions ... The selective 5-lipoxygenase inhibitors, ICI207968, A64077 and BWA4C, and the 5-lipoxygenase translocation inhibitor MK886, decreased leukotriene generation but enhanced TNF production
Schade et al., Int J Immunopharmacol 1991 (Leukopenia...) : Since 5-lipoxygenase inhibitors neither prevented the formation of TNF alpha nor endotoxin leukopenia and lethality, it is suggested that a lipoxygenase product distinct from the leukotrienes is involved in TNF alpha synthesis
MacIntyre et al., Int J Immunopharmacol 1991 : The involvement of protein kinase C, calcium, and 5-lipoxygenase in the production of tumor necrosis factor by a cloned interleukin-3 dependent cell line with natural cytotoxic activity ... Finally, the 5-lipoxygenase inhibitors, ketoconazole and L-656,224, but not the cyclo-oxygenase inhibitor ASA, inhibited TNF stimulated by all agents
Rakkestad et al., Inhal Toxicol 2010 (Inflammation) : Further, we found that the 5-LO inhibitor nordihydrogualaretic acid ( NDGA ) significantly reduced both MEHP induced TNF-alpha release and MEHP induced formation of reactive oxygen species ( ROS ), supporting an involvement of the 5-LO pathway in MEHP induced inflammatory reactions
Piotrowska-Tomala et al., Domest Anim Endocrinol 2012 (Mastitis, Bovine) : Lipopolysaccharides, TNF, IL-1a, and the reagents combination increased PTGS2, PTGES, and PGFS mRNA transcription ( P < 0.01 ), whereas ALOX5 mRNA transcription was increased only by TNF ( P < 0.001 )
Horiguchi et al., Mol Cell Biol 1989 (Leukemia, Promyelocytic, Acute) : Although indomethacin had no detectable effect on this induction of TNF transcripts, ketoconazole, an inhibitor of 5-lipoxygenase , blocked TPA induced increases in TNF mRNA levels
Dubois et al., J Immunol 1989 : Inhibition of 5-lipoxygenase by nordihydro-guaiaretic acid or AA-861 blocked the PAF induced augmentation of both TNF and LTB4 production
Hartman et al., Agents Actions 1993 (Hypersensitivity) : As previously reported, the 5-lipoxygenase/cyclooxygenase (5-LO/CO) inhibitor, SKF86002 ( 30 microM ), significantly inhibited both IL-1 beta and TNF-alpha release using either stimulus
Bureau et al., Eur J Pharmacol 1997 (Bronchopulmonary Sequestration...) : The 5-lipoxygenase inhibitor, BW B70C, injected i.p. ( 30 mg/kg ) prevented leukotriene C4 synthesis by alveolar macrophages and reduced leucocyte migration to the airways lumen as well as albumin microvascular leakage but did not affect the endotoxin induced increase in the blood level of TNF-alpha and of secreted phospholipase A2