Pelargonidin Inhibits Cell Growth and Promotes Oxidative Stress-Mediated Apoptosis in Lung Cancer A549 Cells

Abstract Background: Lung cancer has the worst prognosis with an average 5-year survival rate of only 10-20%. Lung cancer has the highest prevalence rate and a second most common cause of cancer-associated mortalities worldwide. Objective: The present study was planned to explore the anticancer effects of pelargonidin against the lung cancer A549 cells via analyzing oxidative stress-mediated apoptosis. Methodology: The viability of both control and pelargonidin-treated A549 cells was analyzed using the MTT cytotoxicity assay at different time periods. The levels of endogenous ROS generation, mitochondrial membrane potential (Δψm), and apoptosis was assessed using corresponding fluorescent staining assays. The levels of oxidative stress biomarkers including TBARS, SOD, CAT, and GSH in the cell lysates of control and pelargonidin-treated A549 cells was examined using the assay kits. Results: The pelargonidin treatment at diverse concentrations were substantially suppressed the viability of lung cancer A549 cells with an IC50 range of 20 μM for 48 hr. The further treatment with 20 and 40 µM effectively promoted the endogenous ROS production and depleted the Δψm levels in the A549 cells. The outcomes of the dual staining and DAPI staining assays witnessed the occurrence of increased apoptosis in the pelargonidin-treated A549 cells. The pelargonidin also boosted the TBARS and reduced the CAT, SOD, and GSH levels thereby promoted the oxidative stress-regulated apoptosis in the A549 cells. Conclusion: In summary, the findings results of the current study demonstrated an anticancer activity of pelargonidin on A549 cells. The pelargonidin treatment substantially decreased the growth and encouraged the oxidative stress-regulated apoptosis in A549 cells. Therefore, it was evident that the pelargonidin could be employed as an effective anticancer candidate to treat the lung cancer.