Anti-proliferative effects of leaf extract of Petroselinum sativum on human lung and colon cancer cells: Mitochondrial-mediated apoptosis

Plant-derived natural products have attracted considerable attention for their potential in treating human diseases, particularly cancer. This study aimed to evaluate whether the ethanolic Petroselinum sativum ethanolic extract (PS-Et) can inhibit the growth of human lung carcinoma (A-549) and human colon adenocarcinoma (CaCo-2) cell lines. Leaves were extracted with 80% ethanol and tested for effects on cell viability, morphology, reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP) level, caspase enzymes, and apoptosis-related genes. In both cell lines, PS-Et significantly reduced cell viability in a dose-dependent manner, with an IC 50 value of 17.6 μg/mL and 21.2 μg/mL for A-549 and Caco-2 cells, respectively. Further assays on morphology, ROS generation, mitochondrial membrane potential, caspase enzymes, and real-time qPCR were performed in A-549 cells using cytotoxic doses of PS-Et. PS-Et markedly reduced the growth of A-549 and Caco-2 cells and induced notable changes in their morphology. Furthermore, PS-Et dose-dependently increased ROS generation, disrupted mitochondrial function, and activated caspase enzymes in A-549 cells. Mitochondrial-mediated apoptosis was evident, as shown by the increased expression of p53, Bax, caspase-3, and caspase-9, along with decreased expression of the anti-apoptotic gene, Bcl-2. Collectively, PS-Et exerts a potent anticancer effect by promoting mitochondrial dysfunction, oxidative stress, and the intrinsic apoptotic pathway in A-549 cells. These findings suggest that PS-Et extract could serve as a potential therapeutic candidate for combating cancer.