Abstract
The present study aimed to investigate the molecular mechanisms by which paeonol impedes DNA damage repair, induces apoptosis and inhibits cell viability via the mitogen-activated protein kinase (MAPK) pathway. Firstly, normal human bronchial epithelial cells (BEAS-2B) and non-small cell lung cancer cells (H1299) were employed in the study as cellular models. Following cultivation, the cells were divided into experimental and control groups, and were treated with different concentrations of paeonol. Subsequently, various techniques, including western blotting, Cell Counting Kit-8, colony formation, TUNEL and comet assays were conducted to evaluate the effects of paeonol on cell viability, colony-forming ability, apoptosis levels and DNA damage in H1299 cells. According to the experimental results, paeonol significantly reduced the viability and colony formation ability of H1299 cells, but substantially increased apoptosis and DNA damage. These effects were enhanced in response to higher concentrations of paeonol. Furthermore, western blot analysis revealed that paeonol treatment decreased the protein levels of B-cell lymphoma 2 and breast cancer susceptibility gene 1, while it increased the expression levels of cleaved-PARP, cleaved-caspase 3, γH2AX and P21. Additionally, the phosphorylated levels of extracellular signal-regulated kinase 1, c-Jun N-terminal kinase and P38 within the MAPK signaling pathway were diminished. Collectively, the present study demonstrated that paeonol may inhibit the metabolic activity and proliferative capability of H1299 cells, and that it could promote apoptosis and obstruct DNA damage repair by modulating the MAPK signaling pathway.