Inhibition of lung cancer proliferation by wogonin is associated with activation of apoptosis and generation of reactive oxygen species

Abstract

Background: Lung cancer has a very high incidence rate and is one of the commonly diagnosed tumors in developed countries. Aims: To investigate the effect of wogonin on A549 and A427 lung cancer cells and explore the mechanism involved. Study Design: Cell study. Methods: The cytotoxicity effect of wogonin on A549 and A427 lung cancer and BEAS-2B cells was assessed by MTT assay. The onset of apoptosis was assessed by flow cytometry using Annexin V FITC/PI staining. Western blotting was used for the determination of changes in apoptotic protein expression. Results: Wogonin treatment exhibited cytotoxicity effect selectively on A549 and A427 cells without affecting BEAS-2B normal lung cells. The viability of A549 and A427 cells was reduced to 31% and 34%, respectively, on treatment with 50 µM of wogonin; however, there was no significant reduction in BEAS-2B cell viability on treatment with the same concentration of it. Moreover, the percentage of apoptotic A427 cells showed a significant (p<0.049) increase on treatment with wogonin. Furthermore, the treatment led to a marked increase in the activation of caspase 3/8/9 and the generation of reactive oxygen species (ROS) at 72 h in A427 cells. Digital tomosynthesis studies showed a marked reduction in tumor development on treatment with wogonin. Conclusion: Wogonin treatment specifically exhibits a cytotoxic effect on lung cancer cells and this effect is associated with activation of apoptosis and generation of reactive oxygen species.