RESUMEN
Herein, a simple and efficient fluorescence analysis method for L-Cysteine (L-Cys) was established. The method was based on the fluorescent "off-on" mode of nitrogen doped carbon dots (NCDs). The NCDs were prepared via a facile one-step solvothermal method. In the process of exploring the bio-functional application of these newly synthesized NCDs, we found these NCDs with rich functional groups exhibited excellent optical properties. In addition, these newly synthesized NCDs showed an excitation-dependent emissions photolumine-scent (PL) property and exhibited good performance in the detection of Fe3+ ions by quenching the blue emission fluorescence. Interestingly, the quenched fluorescence of NCDs was recovered with the addition of L-Cys, which provided a novel approach for L-Cys detection. The NCDs-based fluorescent "off-on" sensor has a wide linear detection range (0-100 µM), and a relatively low detection limits (0.35 µM) for L-Cys. This simple fluorescent "off-on" approach is, very sensitive and selective for L-Cys detection, which also provides a new insight on NCDs biosensor application.
RESUMEN
A series of experiments have been carried out to investigate the effects of different concentrations of thapsigargin (0, 0.001, 0.1, and 1 µM) on the proliferation and survival of human rheumatoid arthritis synovial cells (MH7A). The results showed that thapsigargin can block the cell proliferation in human rheumatoid arthritis synovial cells in a time- and dose-dependent manner. Results of Hoechst staining suggested that thapsigargin may induce cell apoptosis in MH7A cells in a time- and dose-dependent manner, and the percentages of cell death reached 44.6% at thapsigargin concentration of 1 µM treated for 4 days compared to the control. The protein and mRNA levels of cyclin D1 decreased gradually with the increasing of thapsigargin concentration and treatment times. Moreover, the protein levels of mTORC1 downstream indicators pS6K and p4EBP-1 were reduced by thapsigargin treatment at different concentrations and times, which should be responsible for the reduced cyclin D1 expressions. Our results revealed that thapsigargin may effectively impair the cell proliferation and survival of MH7A cells. The present findings will help to understand the molecular mechanism of fibroblast-like synoviocytes proliferations and suggest that thapsigargin is of potential for the clinical treatment of rheumatoid arthritis.