Catalytical feature of optical nanoprobes of boron nitride quantum dots in the presence of Cu2+ for the determination of dopamine.

Monitoring the concentration of dopamine (DA) is vital for preventing and diagnosing DA related diseases. In contrast to the traditional sensing methods for DA, in which direct or indirect effects on the optical probes are often recorded, a novel sensing concept is disclosed based on as a result of the in situ formation of polydopamine (PDA) originating from the synergetic effect between boron nitride quantum dots (BNQDs) and Cu2+. In the co-presence of BNQDs and Cu2+, DA was catalytically oxidized to PDA, accompanied by an obvious color change from colorless to brown. In contrast to previous reports, in which BNQDs have been employed as an optical probe, herein, the BNQDs not only acted as the optical energy donor, but also as the catalysts for the formation of PDA. The quenching efficiency resulting from the inner filter effect and the electron transfer between the BNQDs and PDA was directly proportional to the concentration of DA, ranging linearly from 2 to 80 µM with a limit of detection of 0.49 µM. The present system exhibited an outstanding selectivity for DA among other interfering coexisting biomolecules. Furthermore, the practical application of the proposed platform was verified by assaying DA in human plasma samples, and satisfactory recoveries ranging from 101.24% to 111.98% were obtained. With the satisfactory reliability, repeatability and stability, the proposed simple sensor showed significant potential for use in DA detection in other biomedical applications.

Ginsenoside Rh2 impedes proliferation and migration and induces apoptosis by regulating NF-κB, MAPK, and PI3K/Akt/mTOR signaling pathways in osteosarcoma cells.

Ginsenoside Rh2 is a primary bioactive compound obtained from ginseng that indicated anticancer activities against several malignant tumors. However, previous studies have reported little about the inhibitory effect of Rh2 on osteosarcoma (OS). This study aims to explore whether Rh2 could exert anticancer effects in OS cells and further investigate the proliferation, migration, and apoptosis mechanisms induced by Rh2 in human OS U20S cell line. The viability of U20S cells was obtained by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay. Cell migration property was analyzed by wound-healing assay. Apoptosis was visualized using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL), 4',6-diamidino-2-phenylindole (DAPI), and annexin V/propidium iodide (PI) staining. Relative protein expressed was confirmed through Western blot analysis. Mitochondrial membrane potential was evaluated by JC-1 staining. In this study, we used broad-spectrum anticancer drug cisplatin (CP) as a positive control. The results indicated that Rh2 remarkably inhibited cell viability of U20S cells in a dose- and time-dependent manner, and suppressed migration. TUNEL, DAPI, annexin V/PI, and JC-1 assay suggested that Rh2 could induce cellular apoptosis. Rh2 could reduce the levels of Bcl-2, caspase 3, and caspase 9, and promote the expression level of Bax in U20S cells. Moreover, Rh2 could induce apoptosis by promoting mitogen-activated protein kinase (MAPK) signaling pathway and inhibit PI3K/Akt/mTOR and nuclear factor-κB (NF-κB) signaling pathway in U20S cells. These findings indicated that Rh2 has an anticancer effect on U20S cells by regulating MAPK, PI3K/Akt/mTOR, and NF-κB signaling pathway.