Modulation of apoptosis in HaCaT keratinocytes via differential regulation of ERK signaling pathway by flavonoids.

摘要: The exact molecular mechanisms underlying the cellular effects associated with various flavonoids have yet to be fully explained. In present study, we administered several human HaCaT keratinocytes and determined that 3,4′-dihydroxy flavone (3,4′-DHF) exerts a slight stimulatory effect on cell growth, although other flavonoids, including kaempferol, quercetin, isorhamnetin, exhibited growth inhibitory properties. 3,4′-DHF was found exert an anti-apoptotic etoposide-induced death of keratinocytes. We were also able determine sustained ERK activation intimately apoptosis cells, treatment induced significant suppression activation, concomitant repression poly(ADP-ribose) polymerase or cleavage pro-caspase 3. overexpression significantly overrode function 3,4′-DHF, but this not true ERK-DN. Moreover, resulted in protection cells from H2O2-induced exerted apparent suppressive stress-induced generation reactive oxygen species (ROS). Finally, showed almost completely abolished kaempferol-induced apoptosis, coupled both intracellular ROS ERK. Taken together, our data clearly indicate host phytochemicals, etoposide variety differentially regulate via differential modulation production, signaling pathway. According these results, are conclude distinct structure-activity relationship between flavonoids.