The relative percentage of apoptotic living cells in the different exper imental setups in K562 and K562 Adr cells, following 48 h treatment method are represented as being a bar graph in Fig. 8. Inter estingly, despite the fact that each cell sorts present comparable early apoptotic cell populations in presence with the distinctive Sia mois polyphenols, late apoptotic cells only accumulate in K562 cells. In contrast to Siamois polyphenols, only withaferin A is able to trigger late apoptosis in K562 Adr cells. In addition, despite the fact that the concentrations utilized from the numerous Siamois polyphenols closely relate for the IC50 values established in MTT assay, FACS evaluation reveals important variation in apoptosis efficacy concerning the different polyphenol compounds.
The latter suggests sizeable discrepancies among MTT cell viability assays exposed by mitochondrial reduction of tetrazolium salts and cell survival score mea sured by Annexin V PI apoptosis FACS assay, Certainly, it really is of utmost significance to perform a variety of, methodologically unrelated assays to quantify dying and dead cells, Next, as apoptotic threshold in compound taken care of K562 Adr cells might be increased great post to read because of elevated basal anti apoptotic activity of NF?B, AP1 and Nrf2, we desired to additional assess whether or not expanding action of NF?B, AP1 and Nrf2 by PMA therapy in K562 cells could sim ilarly shield compound handled K562 cells from late apoptosis in analogy to K562 Adr cells. Even so, even though the relative amount of late BSI201 apoptotic cells decreases on cotreatment of K562 cells with PMA and Siamois polyphenol inhibitors, execution of apop tosis just isn’t entirely blocked simply because Siamois polyphe nols can partially counteract PMA effects on NF?B, AP1 and Nrf2. Along the exact same line, Siamois poly phenols cannot overcome the late apoptosis block in K562 Adr cells, despite effective inhibition of NF?B, AP1 and Nrf2. This suggests that execution of apoptosis in K562 Adr cells is only in part determined by transcrip tional action of NF?B, AP1 and Nrf2.