D-penicillamine modified copper nanoparticles for fluorometric determination of histamine based on aggregation-induced emission.

A fluorometric method for the determination of histamine has been developed based on aggregation-induced emission (AIE) effect of D-penicillamine capped copper nanoparticles (DPA-CuNPs). The fluorescent DPA-CuNPs were synthesized by a one-pot method using D-penicillamine as both reducing agent and stabilizing ligand. The size, morphology and physical chemical properties of DPA-CuNPs were examined by transmission electron microscopy (TEM), fluorescence spectroscopy, fourier transform infrared spectroscopy (FTIR) and absorption spectroscopy. The DPA-CuNPs exhibit AIE effect and show intense red fluorescence (650 nm). In the presence of histamine, DPA-CuNPs are dispersed into small homogeneous particles, causing fluorescence quenching. Based on this reaction, a histamine sensor is constructed. The fluorescence of the CuNPs solution has a good linear relationship with histamine concentration in the range 0.05 µM to 5 µM and the determination limit (3σ/slope) is 30 nM. The estimated method was successfully applied to the determination of histamine in fish, pork and red wine. Graphical abstract Schematic representation of copper nanoparticles for histamine analysis. In the presence of histamine, the strong red fluorescence of copper nanoparticles is obvious decreased through interaction of copper nanoparticles and histamine.

Quercetin suppresses apoptosis of chondrocytes induced by IL-1ß via inactivation of p38 MAPK signaling pathway.

The objective of the present study was to investigate the effect of quercetin and evaluate its protective effect on articular cartilage in patients with osteoarthritis (OA), by intervening the p38 pathway. The target factors of quercetin protecting articular cartilage in patients with OA were predicted scientifically and analyzed to predict the possible pathways by using network pharmacology. A pathway predicted to be closely associated with osteoarthritis was chosen for experimental verification in in vitro cells. The optimal intervention drug concentrations were selected by the of Cell Cycle Kit-8 assay, osteoarthritis and inflammatory factors relevant to osteoarthritis, interleukin-1ß and tumor necrosis factor-α, were tested by of enzyme-linked immunosorbent assay, and the expression of relevant proteins and mRNA of the p38 signaling pathway was tested by reverse transcription-quantitative PCR and western blotting, following quercetin intervention. It was found that quercetin, at the concentration of 100 umol/l, can decrease inflammatory factors relevant to OA, inhibit the expression of p38, matrix metalloprotease 13 and ADAMTS in the pathway, and promote the expression of collagen Ⅱ. Therefore, it is postulated that quercetin can lower the expression of inflammatory factors in cartilage for the prevention and treatment of OA, and the expression level of relevant factors can be changed positively by blocking the p38 MAPK signaling pathway. Thus, quercetin can promote the repair of degenerative chondrocytes and protect articular chondrocytes.