Hepatocellular carcinoma (HCC) is one of the most lethal cancers, and the morbidity and mortality are increasing continuously. Curcumin plays an important role in anticancer activity, while its clinical application is limited by its poor aqueous solubility. To develop an aqueous formulation and improve the anticancer activity of curcumin, curcumin-surface decorated selenium nanoparticles (Se@Cur) were designed in the present study. Transmission electron microscopy (TEM) images and MTT assays indicated Se@Cur dramatically suppressed the proliferation of HepG2 cells and showed low toxicity to normal cells. Compared with SeNPs and curcumin, Se@Cur significantly inhibited the migration ability of HepG2 cells. Moreover, induction of apoptosis in HepG2 cells by Se@Cur was proved by accumulation of the sub-G1 cell population, nuclear condensation and activation of caspase-3. Furthermore, Se@Cur promoted intracellular ROS overproduction and induced apoptosis via activating p53 and AKT signal pathways. Finally, in a xenograft nude mice model, Se@Cur suppressed the growth of tumors. Altogether, the findings in the present study demonstrated the application of Se@Cur as a safe and hopeful strategy for chemotherapeutics of HCC.

Zanamivir is an effective drug for influenza virus infection, but strong molecular polarity and aqueous solubility limit its clinical application.

SeNPs inhibited the apoptosis induced by H1N1 virus infection in MDCK cells by improving the level of GPx1. Our results suggest that SeNPs are an effective selenium source and a promising H1N1 influenza antiviral candidate.

The morbidity and mortality of hepatocellular carcinoma, the most common cancer, are increasing continuously worldwide. Galangin (Ga) has been demonstrated to possess anti-cancer effect, but the efficacy of Ga was limited by its low permeability and poor solubility. To develop aqueous formulation and improve the anti-cancer activity of Ga, surface decoration of functionalized selenium nanoparticles with Ga (Se@Ga) was synthesized in the present study. The aim of this study was to evaluate the anti-cancer effect of Se@Ga and the mechanism on HepG2 cells. Se@Ga-induced HepG2 cell apoptosis was confirmed by depletion of mitochondrial membrane potential, translocation of phosphatidylserine and caspase-3 activation. Furthermore, Se@Ga enhanced the anti-cancer activity of HepG2 cells through ROS-mediated AKT and p38 signalling pathways. In summary, these results suggest that Se@Ga might be potential candidate chemotherapy for cancer.