Molecular Mechanisms of Cigarette Smoke-Induced Proliferation of Lung Cells and Prevention by Vitamin C
Figure 1
AECS/p-BQ-induced proliferation of human lung epithelial cells (A549) and its prevention by anti-p-BQ antibody. Except in (d), all the treatments were made in 24 hr. Effect of concentration gradient of AECS on proliferation and death of A549 cells in culture, as determined by MTT cytotoxicity assay (a). AECS (2 μL/mL) or p-BQ (200 ng/mL)-induced proliferation in other cell lines, namely. L132, Vero, and HepG2 (b). Effect of concentration gradient of p-BQ on proliferation and death of A549 cells in culture, as determined by MTT cytotoxicity assay (c). Treatment with AECS (2 μL/mL) or p-BQ (200 ng/mL) results in continued proliferation for 24–72 hr (d). AECS/p-BQ-induced proliferation is prevented by anti-p-BQ antibody, as evidenced by MTT assay (e). The inhibitory role of anti-p-BQ antibody on the proliferation of A549 cells as determined by the incorporation of BrdU using flow cytometry assay (f, g). All data are depicted as the mean ± SD for three independent experiments (* indicates significant difference, in comparison to nontreated control (a, b, c, d); and in comparison to AECS and p-BQ, resp. (e, g)).
