THE EFFECT OF BOSWELLIC ACID ON ROS PRODUCTION AND CASPASE-DEPENDENT APOPTOTIC PROCESSES IN SUPPRESSION OF HELA CELL GROWTH

Abstract

Objective: Boswellic acid (BA), a pentacyclic triterpenoid derived from Boswellia species, has attracted attention for its anti-inflammatory and anticancer properties. This study investigated the anticancer effects of BA in human cervical cancer HeLa cells and explored the underlying molecular mechanisms.Methods: Cell viability was evaluated using the MTT assay, while apoptosis was assessed by Annexin V/PI flow cytometry. Bax and Bcl2 gene expression was analyzed by quantitative real-time PCR (qRT-PCR). Intracellular reactive oxygen species (ROS) levels and caspase-3/caspase-9 activities were measured to characterize apoptotic mechanisms. STRING-based bioinformatics analysis was performed to identify biological processes and signaling pathways associated with the experimental findings.Results: BA significantly decreased HeLa cell viability in a dose- and time-dependent manner, with a 48 h IC₅₀ of 38.7 μM. BA treatment significantly increased apoptotic cell death, upregulated Bax, and downregulated Bcl2, resulting in an increased Bax/Bcl2 ratio. BA also significantly enhanced intracellular ROS production and caspase-3 and caspase-9 activities, indicating activation of the intrinsic mitochondrial apoptotic pathway. STRING analysis supported these findings, revealing enrichment of apoptosis-, oxidative stress-, and cell cycle-related processes and pathways.Conclusion: BA induces apoptosis in HeLa cells through ROS generation, modulation of the Bax/Bcl2 balance, and activation of the mitochondrial caspase cascade. These findings support the potential of BA as a natural anticancer compound and warrant further in vivo preclinical investigation.