The induction of apoptosis was substantially enhanced by increasing the dose of flavonoids, and more improved by prolonging treatment time from 72 h to 96 h. In this case, baicalein and baicalin produced the highest amounts of apoptosis in U87 MG cells, followed by wogonin, apigenin, chrysin and scutellarein, in accordance. Nonetheless, the examine did not report any specifics with regards to the apoptotic activity of chrysin and other flavonoids in U 251, MDA MB 231 and PC3 cells. Other research have reported the results of chrysin, like in NSCLC and colon carcinoma. For example, chrysin, have been reported to have prospective as adjuvant treatment for drug resistant NSCLC, specially in sufferers with AKR1C1/1C2 overexpression.

This examine evaluated the influence of flavonoids and demonstrated that IL 6 induced AKR1C1/1C2 overexpression and drug resistance can be inhibited by chrysin and wogonin, which both demonstrated NSCLC multiple antiinflammatory effects in these cells. Chrysin has also been demonstrated to lead to SW480 cells to arrest at the G2/M phase of the cell cycle in a dose dependent manner. Combining chrysin with apigenin was located to double the proportion of SW480 cells in G2/M. Thus, apigenin relevant flavonoids this kind of as chrysin, may possibly cooperatively protect towards colorectal cancer by way of conjoint blocking of cell cycle progression. Chrysin also inhibited the lipopolysaccharide induced COX 2 expression by way of inhibition of nuclear aspect IL 6.

Thus, chrysin might also enhance the drug sensitivity of cancer cells by modulating the signaling pathways of inflammatory cytokines. Perhaps the biological activities of chrysin could be enhanced by mixture with other flavonoids, as combinations of flavonoids have been demonstrated to have greater apoptotic effects than personal Paclitaxel use of chrysin. For illustration, the blend of Factot Xa with apigenin, baicalin and scutellarein inhibited the proliferation of U87 MG glioma cells by almost 50%, whilst chrysin alone showed no anti proliferative activity in these cells. In addition to, modified chrysin is demonstrated to exhibit much more powerful anti cancer results than the unmodified chrysin.

In addition to the inhibitory results of phosphorylated chrysin antigen peptide in HeLa cells, as talked about above, 5 allyl 7 gen difluoromethylenechrysin has proven to inhibit the proliferation of human ovarian cancer cells, CoC1, in a dose dependent manner. The ADFMChR substantially induced apoptosis in this cell line in a concentration dependent manner, with rates of apoptosis of 33. 07% and 73. 70% following the cells were treated with ten. and 30. umol/L of ADFMChR, respectively, for 48 h. The apoptosis fee was compared with the cells handled with 10. and 30. umol/L of unmodified chrysin, which rates the apoptosis of 21. 70% and 40. 00%, respectively. Moreover, another study investigating the results of 5,7 dihydroxy 8 nitrochrysin on apoptosis in human gastric carcinoma cell line, SGC 7901, showed that NOChR markedly inhibited the proliferation of SGC 7901 cells in a dose dependent manner, in which the potency of NOChR was ten occasions increased than that of unmodified chrysin.

All round, all these reports suggest that modified chrysin could exhibit more strong anti cancer effects than the unmodified chrysin. It is also attainable that the potency of chrysin is enhanced by addition of more antigen peptide constituents. According to Monasterio et al. , at least two hydroxyls at positions 3, 5 or 7 of the A ring have been required to confer the pro apoptotic activity.