Effect of NADPH oxidase inhibitor apocynin on human lung cancer A549 cells via Bcl-2, Bax, caspase-3, and NF-κB signaling pathway.

Apocynin (AP) is an anti-inflammatory drug with different therapeutic effects. This study aimed to investigate the antiproliferative, apoptotic, and antioxidant effects of AP on human lung adenocarcinoma cells (A549) and to investigate the effects on Bax, Bcl-2, NF-κB, and caspase-3 signaling pathways that may play a role in the pathogenesis of lung cancer. Cell viability was measured by MTT and cell apoptosis, and detection of cell death was measured by ELISA. IMA, AOPP, MDA, and GSH levels, SOD and CAT activities, and Bcl-2, Bax, NF-κB, and caspase-3 expression levels were analyzed from the obtained cell lysates. As a result, according to the findings obtained, IMA and MDA levels decreased in the A549 cancer cell line, while GSH levels and SOD and CAT activity increased. It was determined that the application of apocynin to A549 cells significantly reduced cell viability and directed the cells to apoptosis, increased Bax, NF-κB, and caspase-3 expression, and decreased Bcl-2 expressions. Since all of the data obtained were not found in the literature about the use of apocynin in the A549, the study conducted is pioneering. Our study demonstrates the potential of apocynin for cancer therapy possibly targeting the apoptotic pathway.