Inhibitory effect of linomide on lipopolysaccharide-induced proinflammatory cytokine tumor necrosis factor-alpha production in RAW264.7 macrophages through suppression of NF-κB, p38, and JNK activation

Saucerneol F, a new lignan, inhibits iNOS expression via MAPKs, NF-κB and AP-1 inactivation in LPS-induced RAW264.7 cells

“…It is well established that iNOS expression by LPS in macrophages is regulated by the transcription factors nuclear factor-κB (NF-κB) and AP-1 [10]. In parallel, LPS stimulates phosphorylation of inhibitor κB (IκB) resulting in its degradation and activated translocation of NF-κB to the nucleus [11][12][13]. LPS activates mitogen-activated protein kinases (MAPKs) such as extracellular signal-regulated kinases (ERK) 1 and 2, c-Jun N-terminal kinase (JNK), and p38.…”

Saucerneol D, a naturally occurring sesquilignan, inhibits LPS-induced iNOS expression in RAW264.7 cells by blocking NF-κB and MAPK activation

“…The reactive radical, NO, generated by iNOS, is a major inflammatory mediator produced by macrophages and is involved in development of inflammatory processes [19]. Here, SD isolated from S. chinensis inhibited NO production and iNOS protein expression in a concentration-dependent manner in LPS-stimulated RAW264.7 cells (Fig.…”

“…The neural (nNOS) and endothelial (eNOS) isoforms are constitutively expressed in select tissues, and their enzymatic activity is regulated by changes in the intracellular free Ca 2+ concentration [14,15]. A third member of the NOS family is inducible NOS (iNOS), which is produced in large quantities in response to inflammatory stimuli, such as LPS, interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α) [16][17][18][19]. NO is also involved in pathophysiological processes such as atherosclerosis, inflammation, and carcinogenesis [20,21].…”

Japanese Apricot (Ume): A Novel Therapeutic Approach for the Treatment of Periodontitis

“…Therefore, blockade of TNF-α and IL-6 secreted by periodontal pathogens or other cytokines may suppress pro-inflammatory responses, and inhibit the development and progression of periodontal disease. It has been reported that LPS possibly induces TNF-α and IL-6 expressions through transient phosphorylation of ERK1/2, JNK, and p38MAPK (Matsuzaki et al, 2004;Kim et al, 2007;Son et al, 2008;Neuder et al, 2009;Xiao et al, 2007). Additionally, it has been also reported that the production of inflammatory cytokines requires nuclear factor kappaB (NF-κB) activation (D'Acquisto et al, 1997).…”