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. 2021 Mar 10;6(11):7815–7828. doi: 10.1021/acsomega.1c00308

Figure 4.

Figure 4

BBT activates JNK-, p38-, and caspase-dependent apoptosis. (A) Cell cycle histograms of Hela cells after treatment with various concentrations of BBT. Analysis of apoptosis using the annexin V and PI method. (B) HeLa cells were incubated in the absence (control) or presence of BBT (12.5 μM). Then, cell death was analyzed using annexin V and PI through flow cytometry. (C) Flow-cytometric analysis of mitochondrial membrane potential (ΔΨm) with the help of JC-1 staining in treated and untreated samples.(D) Immunoblotting analysis of cell lysates collected from HeLa cells after treatment of 12.5 μM BBT. Stress response pathway (p-JNK1/2, p-c-jun, and p-p38) and apoptotic factors (cleaved caspase 9 and 3 and PARP) were seen to be upregulated on treatment with BBT. α-Tubulin was used as a loading control. All experiments have been performed thrice (n = 3). PI: propidium iodide, PARP: poly(ADP-ribose) polymerase, and JNK: Janus kinase.