ABSTRACT
Nitric oxide (NO) is a short-lived, small, highly diffusible, reactive, free radical gas, ubiquitous bioactive molecule, and is derived from L-arginine (a well-known amino acid). This constituent was discovered 30 years back as “endothelium-derived relaxing factor.” In mammalian cells, NO acts as a mediator and is believed to play a crucial function in several biological processes. The current chapter comprehensively highlights the emerging perspectives of natural chalcone-based nitric acid inhibitors such as sofachalcone, brussochalcone A, cardamonin, flavokawain B, dimethyl cardamonin (2′,4′-dihydroxy-6′-methoxy-3′,5′-dimethylchalcone), mallotophilippens, Hidabeni chalcone, okanin, sappanchalcone, 3-deoxysappanchalcone, 2′,4′,6′-tris(methoxymethoxy) chalcone, butein, and 2licochalcone A which selectively inhibited the production of NO (inducible NO synthase, neuronal NO synthase, and endothelial NO synthase), cytokine, interleukin, TNF-α, MCP-1, and prostaglandins by preventing the phosphorylated IκBα-induced translocation of NF-κB p65 subunit at nuclear milieu, inhibition of NF-κB functions, inhibiting LPS-induced translocation by Erk-1/2 MAP-kinase phosphorylation, restricting the STAT1 expression, and inducing the expression of heme oxygenase-1 (HO-1) by activation of AKT/mTOR pathway in LPS-stimulated RAW 264.7 cells and 3T3-F442A adipocytes.
