Dendropanax morbifera Léveille is an oriental medicinal plant that is traditionally used in folk medicine and grows in a specific region of South Korea. We aimed to enhance the utilization of D. morbifera medicinal plants for synthesis of silver nanoparticles (AgNPs) and gold nanoparticles (AuNPs). D. morbifera leaf extract acted as both a reducing and a stabilizing agent that rapidly synthesized Dendropanax AgNPs (D-AgNPs) and Dendropanax AuNPs (D-AuNPs). The D-AgNPs and D-AuNPs were characterized by ultraviolet-visible spectroscopy, energy dispersive X-ray analysis, elemental mapping, field emission transmission electron microscopy, X-ray diffraction, and dynamic light scattering. The characterizations revealed that the D-AgNPs and D-AuNPs were in polygon and hexagon shapes with average sizes of 100–150 nm and 10–20 nm, respectively. The important outcomes were the synthesis of AgNPs and AuNPs within 1 hour and 3 minutes, respectively, avoiding the subsequent processing for removal of any toxic components or for stabilizing the nanoparticles. Additionally, D-AgNPs and D-AuNPs were examined for cytotoxicity in a human keratinocyte cell line and in A549 human lung cancer cell line. The results indicated that D-AgNPs exhibited less cytotoxicity in the human keratinocyte cell line at 100 µg/mL after 48 hours. On the other hand, D-AgNPs showed potent cytotoxicity in the lung cancer cells at the same concentration after 48 hours, whereas D-AuNPs did not exhibit cytotoxicity in both cell lines at the same concentration. However, both D-AgNPs and D-AuNPs at 50 µg/mL enhanced the cytotoxicity of ginsenoside compound K at 25 µM after 48 hours of treatment compared with CK alone. We believe that this rapid green synthesis of D-AgNPs and D-AuNPs is a valuable addition to the applications of D. morbifera medicinal plant. D-AuNPs can be used as carriers for drug delivery and in cancer therapy due to their lack of normal cell cytotoxicity.

Background: Zinc oxide nanoparticles (ZnO NPs) are used in modern cancer therapy based on their specific target, efficacy, low toxicity and biocompatibility. The photocatalytic performance of Zinc oxide (ZnO) nanocomposites with hyaluronic acid (HA) was used to study anticancer properties against various human cancer cell lines. Methods: Zinc oxide (ZnO) nanocomposites functionalized by hyaluronic acid (HA) were prepared by a co-precipitation method (HA-ZnONcs). The submicron-flower-shaped nanocomposites were further functionalized with ginsenoside Rh2 by a cleavable ester bond via carbodiimide chemistry to form Rh2HAZnO. The physicochemical behaviors of the synthesized ZnO nanocomposites were characterized by various analytical and spectroscopic techniques. We carried out 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay to evaluate the toxicity of Rh2HAZnO in various human cancer cells (A549, MCF-7, and HT29). Furthermore, to confirm the apoptotic effects of Rh2HAZnO and to determine the role of the Caspase-9/p38 MAPK pathways by various molecular techniques such as RT-PCR and Western blotting. Furthermore, Rh2HAZnO induced morphological changes of these cell lines, mainly intracellular reactive oxygen species (ROS) were observed by ROS staining and nucleus by Hoechst staining. Results: We confirmed that Rh2HAZnO exhibits the anti-cancer effects on A549 lung cancer, HT29 colon cancer, and MCF7 breast cancer cells. Moreover, intracellular reactive oxygen species (ROS) were observed in three cancer cell lines. Rh2HAZnO induced apoptotic process through p53-mediated pathway by upregulating p53 and BAX and downregulating BCL2. Specifically, Rh2HAZnO induced activation of cleaved PARP (Asp214) in A549 lung cancer cells and upregulated Caspase-9/phosphorylation of p38 MAPK in other cell lines (HT29 and MCF-7). Furthermore, Rh2HAZnO induced morphological changes in the nucleus of these cell lines. Conclusion: These results suggest that the potential anticancer activity of novel Rh2HAZnO nanoparticles might be linked to induction of apoptosis through the generation of ROS by activation of the Caspase-9/p38 MAPK pathway.