-dependent inhibition of cell proliferation, suggesting that the nutmeg extract inhibited the proliferation of KB cells. The extract was capable to decrease the expression of your bcl-2 gene in cells, diminishing the expression of this protein and inducing early and late apoptosis. Additionally, the cells shrank and showed morphological adjustments when analyzed below a microscope. Cancer cells, having said that, exhibit resistance to apoptosis to be able to sustain their uncontrolled proliferation, and for that reason any compound that modulates apoptosis is desirable as a plausible cancer chemotherapy agent [37]. Pure and partially purified myristicin obtained from Myristica fragrans have been tested against human rhabdomyosarcoma (RD) cells in vitro. At reduce concentrations and inside the very first 24 h of therapy, cell growth inhibition had a important distinction: the partially purified extract showed a higher inhibitory activity. However, after 48 h of therapy and at concentrations above 125 /mL, each MNK1 Accession extracts showed a comparable inhibitory activity. The highest rate of inhibition was 82.3 , reported in the concentration of 500 /mL of pure myristicin. For that reason, it is actually suggested that the extraction approach may possibly interfere with theMolecules 2021, 26,six ofbiological impact; nevertheless, myristicin showed cytotoxic/antiproliferative activity for the studied strain [39]. The vital oil of Myristica fragrans containing 32 myristicin was capable to induce a substantial reduction in human colorectal adenocarcinoma cells (Caco-2) cell viability in the concentration of 250 /mL. In addition, myristicin isolated from the oil showed an IC50 worth of 146 /mL, indicating that it could be the substance responsible for the cytotoxic activity of the oil [36]. Pure myristicin is also capable of inhibiting the development of AA8 and EM9 ovarian cells. Cell viability assays have been performed just after therapy with unique concentrations of myristicin (from 50 to 2000 ) for 24 h, working with the MTT assay protocol. The results showed a reduction in viability. Other assays were carried out, and the benefits showed that myristicin induced cell apoptosis via the activation of caspases (as currently reported by other authors) in each strains, but mainly in EM9. Having said that, it was not able to induce DNA damage [40]. Among the in vitro studies compared the cytotoxicity of myristicin and its active metabolite, 1′-hydroxymyristicin, against HepG2 cells, a human hepatocellular carcinoma line. Cells exposed to myristicin for 24 h did not show a considerable reduction in cell viability. In contrast, cells exposed to 1′-hydroxymyristicin, inside the same concentration variety, showed a dramatic reduction in viability inside the MTT test. A significant enhance within the number of apoptotic cells (each in the early and late stages of apoptosis) was observed in cells exposed to 1′-hydroxymyristicin. These benefits indicate that the active metabolite of myristicin is possibly extra cytotoxic and apoptotic than the substance itself [41]. Benjakul extract, a standard medicine composed of extracts of Piper chaba, Piper sarmentosum, Piper interruptum, Plumbago indica and Zingiber officinale, which includes 3.5 mg/g of myristicin, was tested for its antiproliferative activity against human tiny cell lung cancer (NCI-H1688) and SIK3 list non-tumor human lung fibroblast cell line (MRC-5). In vitro assays have shown that benjakul is selective and can kill cancer cells with the NCI-H1688 lineage much more than non-tumor cells (MRC-5). Even so, the isolated m
