Synthesis and Characterization of Q0-Eugenol Nanoemulsion for Drug Delivery to Breast and Hepatocellular Cancer Cell Lines

合成和表征Q0-丁香酚纳米乳剂用于乳腺癌和肝癌细胞系的药物递送

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Abstract

Cancer is the second cause of death globally. The advent of nanoparticles has revolutionized drug delivery in cancer treatment. This study introduces a novel Q0-eugenol nanoemulsion designed for enhanced drug delivery. Synthesis of nanoemulsion was performed by the homogenization technique and ultrasonication for size reduction. DLS, FTIR, and UV-vis spectroscopy were used for characterization of Q0-eugenol nanoemulsion. MTT assay and flow cytometry assay were applied to determine the fibroblast, KPL1, and PLC/PRF/5 cell lines to consider the cell viability and apoptosis percentage, respectively. The oxidative status of Q0-eugenol nanoemulsion was evaluated by the ferric reducing antioxidant power assay and the thiobarbituric acid reactive substance assay. The zeta potential charge of eugenol and Q0-eugenol nanoemulsion formulation was equal to 45.1 and 22.7 mV, respectively. Eugenol nanoemulsion and Q0-eugenol nanoemulsion treatment exhibited antiproliferative effect against breast and liver cancer cell lines (p < 0.05). Eugenol nanoemulsion and Q0-eugenol nanoemulsion induced apoptosis through reactive oxygen species-dependent mechanism. Apoptosis rates for PLC/PRF/5 treated with eugenol nanoemulsion, Q0, and Q0-eugenol nanoemulsion were 26.7, 84.7, and 16.8%, respectively. Apoptosis rates for fibroblasts treated with eugenol nanoemulsion, Q0, and Q0-eugenol nanoemulsion were 22.6, 37.8, and 24.4%, respectively. Moreover, in the KPL1 cell line, the apoptosis rates were reported as 11.1, 57.9, and 19% with eugenol nanoemulsion, Q0, and Q0-eugenol nanoemulsion treatments, respectively. Eugenol nanoemulsion and Q0-eugenol nanoemulsion exhibited similar antiproliferative mechanisms against both cell lines. In conclusion, our results showed eugenol nanoemulsion and Q0-eugenol nanoemulsion as a potential treatment option against hepatocellular and breast cancer via induced ROS and apoptosis.

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