Multiple heteroatom dopant carbon dots as a novel photoluminescent probe for the sensitive detection of Cu2+ and Fe3+ ions in living cells and environmental sample analysis.

Heavy metal ion pollution harms human health and the environment and continues to worsen. Here, we report the synthesis of boron (B), phosphorous (P), nitrogen (N), and sulfur (S) co-doped carbon dots (BP/NS-CDs) by a one-step facile hydrothermal process. The optimum synthetic parameters are of 180 °C temperature, 12 h reaction time and 15% of PBA mass. The as-synthesized BP/NS-CDs exhibits excellent water solubility, strong green photoluminescence (PL) at 510 nm, and a high quantum yield of 22.4%. Moreover, BP/NS-CDs presented high monodispersity (7.2 ± 0.45 nm), excitation-dependent emission, PL stability over large pH, and high ionic strength. FTIR, XRD, and XPS are used to confirm the successful B and P doping of BP/NS-CDs. BP/NS-CD photoluminescent probes are selectively quenched by Cu2+ and Fe3+ ions but showed no response to the presence of other metal cations. The PL emission of BP/NS-CDs exhibited a good linear correlation with Cu2+ and Fe3+ concentrations with detection limits of 0.18 µM and 0.27 µM for Cu2+ and Fe3+, respectively. Furthermore, the HCT116 survival cells kept at 99.4 ± 1.3% and cell imaging capability, when the BP/NS-CDs concentration is up to 300 µg/mL by MTT assay. The proposed sensor is potential applications for the detection of Cu2+ and Fe3+ ions in environmental water samples.

Cinnamic acid, from the bark of Cinnamomum cassia, regulates glucose transport via activation of GLUT4 on L6 myotubes in a phosphatidylinositol 3-kinase-independent manner.

BACKGROUND: Cinnamomum cassia (Family: Lauraceae) is an Ayurvedic medicinal plant used traditionally for the treatment of a number of diseases, including diabetes. The hypoglycemic effect of this plant has been established in vivo. However, the effects of cinnamic acid, isolated from C. cassia, on the insulin signaling cascade in an in vitro model have not been elucidated. Hence, the aim of the present study was to evaluate the anti-diabetic effect of cinnamic acid on glucose transport by L6 myotubes. METHODS: The mechanism of action of cinnamic acid was determined using specific targets in the insulin signaling pathway, including protein tyrosine phosphatase (PTP) 1B, phosphatidylinositol 3-kinase (PI3-K) and the glucose transporter GLUT4. After differentiation of myoblast to myotubes, the cells were serum deprived for 5 h and then treated with 1 ng/mL cinnamic acid and 50 µmol/L rosiglitazone for 18 h and 100 nmol/L insulin for 20 min for gene expression studies. RESULTS: Expression of GLUT4 mRNA was increased following treatment of L6 myotubes with 1 ng/mL cinnamic acid. Furthermore, cinnamic acid inhibited PTP1B activity (by 96.5%), but had no significant effect on PI3-K activity. CONCLUSION: On the basis of the results of the present study, we postulate that cinnamic acid isolated from the hydro-alcoholic extract of Cinnamomum cassia activates glucose transport by a PI3-K-independent pathway. However, the detailed mechanism of action requires further analysis.