Fig 1.
Schematic preparation of carbazole ECAP in Cl3/Ethanol, reflux, 5 h RT.
Fig 2.
Characterization of the novel (Z)-4-((9-ethyl-9H-carbazol-3-yl) amino) pent-3-en-2-one (ECAP).
(A) IR, (B) 1H-NMR and (C) 13C-NMR spectrums.
Fig 3.
Dose-response curve showing the cytotoxic effect of ECAP and ellipticine on PBMCs and A549 lung cancer cell line.
(A) The effect of (A) ECAP and (B) ellipticine on cell viability of PBMCs and A549 cells after 24 h treatment. [N = 3 replicates at 95% confidence interval].
Table 1.
IC50 values of ECAP and ellipticine on A549 lung cancer cell line after 24 h treatment.
Fig 4.
The effect of ECAP on lipid peroxidation on A549 lung cancer cells after 24 h incubation.
(p < 0.0002) [*** significance compared to the control, number of replicates: n ≥ 3].
Fig 5.
Comet assay showing DNA damage in A549 cells after 24 h treatment.
(A) Control and (B) ECAP treated A549 cells. (p < 0.0001).
Fig 6.
Western blot data shwing effect of the novel ECAP on protein expression in A549 lung cancer cell line.
(A) Bax, (B) Bcl-2, (C) p53, (D) Nrf2, (E) Hsp70 and (F) SOD.
Fig 7.
Time dependent effect of ECAP on caspase activity and ATP level.
(A) The activity of Caspase-3/7 (6 h: p < 0.4036, 24 h: p < 0.0003), (B) Caspase-8 (6 h: p < 0.4364, 24 h: p < 0.0001), (C) Caspase-9 (6 h: 0.4171, 24 h: p < 0.0124) and (D) ATP (6 h: 0.4011, 24 h: 0.0011) levels in A549 lung cancer cell line after 6 h and 24 h incubation. [* denotes statistical significance with respect to the control and uncertainties represent standard deviation (SD) from the means. Number of replicates: n ≥ 3].
Fig 8.
The effect of ECAP on the induction of apoptosis of A549 cells after 24 h treatment.
[(p < 0.0001), *** significance compared to the control and number of replicates: n ≥ 3].
Fig 9.
A schematic summary of apoptotic pathway of a novel carbazole compound (Z)-4-[9-ethyl-9aH-carbazol-3-yl) amino] pent-3-en-2-one on A549 lung cancer cells.