Aptamer based fluorometric ß-lactoglobulin assay based on the use of magnetic nanoparticles and carbon dots.

The authors describe a fluorometric aptamer based assay for detecting ß-lactoglobulin by using carbon dots (C-dots) as a signal indicator. The aptamer was immoblized on magnetite (Fe3O4) nanoparticles (MNPs), and the C-dots served as a label for the complementary oligonucleotide (cDNA). The assay is based on the hybridization that takes place between aptamer and cDNA. In the presence of ß-lactoglobulin (ß-LG), the aptamer preferentially binds to ß-LG, and this leads to a partial release of the C-dots-cDNA into the solution. After magnetic separation, the supernatant of the solution contains the released C-dots-cDNA which are quantified by fluorometry, best under excitation/emission wavelengths of 354/447 nm. Under the optimal conditions, the fluorescence intensity is proportional to the logarithm of the ß-LG concentration in the 0.25 to 50 ng mL-1 range, with a 37 pg mL-1 detection limit. The method was successfully applied to the determination of ß-LG in hypoallergenic formulations, and the results demonstrated that this assay is a promising tool in food quality control. Conceivably, it also provides the opportunity for detection of other analytes. Graphical abstract Schematic of a novel aptamer based fluorometric ß-lactoglobulin assay based on the use of magnetite (Fe3O4) nanoparticles (MNPs) and carbon dots (C-dots). C-dots were used as a signal indicator and Fe3O4 MNPs acted as a magnetic separator. This assay exhibits high sensitivity and selectivity with a detection limit as low as 37 pg mL-1.

Baicalin protects human fibroblasts against ultraviolet B-induced cyclobutane pyrimidine dimers formation.

Exposure to ultraviolet B (UVB) irradiation is a major risk factor for the development of skin cancer. Therefore, it is important to identify agents that can offer protection against UVB-caused DNA damage. Photocarcinogenesis is caused largely by mutations at the sites of incorrectly repaired DNA photoproducts, of which the most common are the cyclobutane pyrimidine dimers (CPDs). In this study, a DNA damage model of UVB irradiation-induced fibroblasts was established. The immunocytochemical staining, immuno dot blotting and Western blotting were employed in the study. We demonstrated that pre-treatment of fibroblasts with Baicalin dose-dependently reduced the amount of UVB-generated CPDs. Compared with UVB irradiated cells, UVB-induced p53 accumulation was less pronounced in Baicalin-treated cells. Taken together, these results suggest that Baicalin prevent CPDs formation induced by UVB. Baicalin is therefore a promising protective substance against UVB radiation.