Newly Synthesized Imidazoline Compound Regulates Apoptosis and Toll-Like Receptor Signaling in Lung Adenocarcinoma and Normal Epithelial Cells

Imidazoline is a heterocyclic compound with biological activity in regulating apoptosis, inflammation, and immune signaling. Lung cancer is a leading cause of cancer-related death, emphasizing the need for new therapies. This study examined the effects of imidazoline on apoptosis and Toll-like receptor (TLR) expression in A549 lung adenocarcinoma cells and Beas-2B normal bronchial epithelial cells. The chemical structure of the synthesized imidazoline was confirmed by FT-IR spectroscopy. Cells were treated with imidazoline, and expression of apoptotic markers (BAX, BCL-2) and TLR1-10 genes was analyzed. In A549 cells, imidazoline increased BAX and decreased BCL-2, indicating activation of intrinsic apoptosis and cell cycle arrest. Beas-2B cells showed the opposite pattern, suggesting selective toxicity toward cancer cells. Imidazoline also modulated several TLRs in both cell lines, highlighting potential immunoregulatory effects. These findings demonstrate that imidazoline promotes apoptosis and alters immune-related signaling in lung cancer cells without harming normal epithelial cells. This study is the first to report imidazoline’s impact on TLR expression in lung cancer, supporting its potential as a dual anticancer agent targeting both cell death and immune pathways.