Research Paper Volume 8, Issue 11 pp 2915—2926

Figure 2. PL kills SCs by apoptosis. (A) Representative flow cytometric plots to measure apoptotic WI-38 IR-SCs at 48 h after treatment with vehicle (Veh), 10 µM PL, 10 µM Q-VD-Oph (QVD), or the combination of PL and QVD. (B) Quantification of the percentage of viable (gate II: PI⁻ Annexin V⁻) and apoptotic (gates III and IV: PI⁻ Annexin V⁺ and PI⁺ Annexin V⁺) (right) IR-SCs 48 h after treatment as in (A) (left), and quantification of the percentage of viable IR-SCs 72 h after treatment as in (A) (right). (C) Representative western blot and quantitative analysis of cleaved-poly(ADP-ribose) polymerase (cPARP), procaspase-3 (Procasp-3), cleaved caspase-3 (cCasp-3), and β-actin in NCs and WI-38 IR-SCs 24 h and 48 h after incubation with Veh or 10 µM PL. (D) Representative western blot analysis of RIP1, RIP3, and β-actin in WI-38 NCs and IR-SCs 24 h after incubation with Veh or 10 µM PL. A cell lysate of etoposide-treated Jurkat cells was used as a positive control. Data are represented as the mean ± SEM.