CR and ELISA, as well as in vivo, usingis oneand ear edema RelA/p65 medchemexpress reduction assays in mice. the cyclooxygenase two (COX-2) enzyme, which paw of these responsible for the production Furthermore, a However, it didn’t show this activity at mRNA and protein in a position when of prostaglandins.molecular docking study revealed that myristicin would belevels to nontreated in human liver cancer cells [248].Molecules 2021, 26,five ofThe anti-inflammatory activity of myristicin may also happen via other pathways (Figure 2). This molecule is also capable of inhibiting quite a few cytokines and mediators responsible for the chemotaxis of the inflammatory method, for example: tumor necrosis element alpha (TNF-a), interleukins (IL-1, IL-6, IL-8, IL-10 and IL-17), nitric oxide (NO), macrophage inflammatory proteins (MIP-1 r MIP-1), colony stimulating aspect (GM-CSF), IP-10, MCP1 and MCP-3 and myeloperoxidase (MPO). This inhibition happens both at the protein level and in the mRNA regulation level. In vitro research have shown that the inhibition of these cytokines was capable to block the migration and development of neutrophils and macrophages, although in vivo, it promoted a reduction in mice paw edema [16,24,294]. The analgesic action of myristicin has also been evaluated. Tests carried out with Pycnocycla bashagardiana critical oil containing myristicin didn’t lead to analgesic activity in hot plate tests with mice, regardless of its good anti-inflammatory action (reduction of paw edema). The vital oil of Illicium lanceolatum, in addition to its anti-inflammatory activity in vivo (reduction of ear edema), also showed reduced writhing in mice soon after pain induction by acetic acid, indicating a attainable analgesic action. In this case, nonetheless, the author attributes the activity for the association amongst myristicin along with other components with the necessary oil [29,33]. Although a lot of results were obtained through tests with crucial oils containing other substances that will contribute for the anti-inflammatory action, myristicin was the major component in most of them. From these final results, its anti-inflammatory activity in numerous pathways of your inflammation procedure is outstanding. 2.4. Antiproliferative Activity The antiproliferative activity of myristicin has been studied in recent years. Literature data report that myristicin is accountable for the anticancer activity of some medicinal plants and is usually a cancer chemopreventive agent [358]. Athamanta sicula crude μ Opioid Receptor/MOR site extract and isolated myristicin have been tested in vitro for their antiproliferative activity, at a concentration of one hundred /mL, against K-562 (human chronic myeloid leukemia), NCI-H460 (human non-small cell lung adenocarcinoma) and MCF-7 (human breast adenocarcinoma) cells applying the methyltetrazolium (MTT) assay. The extracts and isolated myristicin showed considerable antiproliferative activity within the tested cancer cell lines, with inhibition of 50 to one hundred of cells at various concentrations. Other assays had been employed to investigate the mechanisms of development inhibition, and it was concluded that myristicin induced cell apoptosis by way of alterations in mitochondrial membrane prospective, cytochrome C release, caspase-3 activation, PARP cleavage and fragmentation of DNA. Gene expression profiling revealed a general down-regulation of DNA harm response genes right after exposure to myristicin [35,38]. Exposure of the KB cell line (human oral epidermal carcinoma) using a variable concentration of Myristica fragrans extract (nutmeg) resulted within a concentration
