A sandwich-type electrochemical immunosensor based on spherical nucleic acids-templated Ag nanoclusters for ultrasensitive detection of tumor biomarker.

The accurate determination of tumor biomarkers in blood is of vital significance in the diagnosis and therapy of tumor disease. In this research, an innovative sandwich-type electrochemical immunosensor is designed for the ultrasensitive determination of tumor biomarker AFP using spherical nucleic acids-templated silver nanoclusters (AgNCs) sensing platform. For this purpose, on one hand, DNA functionalized gold nanoparticles (AuNPs@DNA) is selected not only as the cross-linker to immobilize the primary antibody (anti-AFP antibody 1, Ab1) to obtain AuNPs@DNA-Ab1, but also as the template for synthesizing AgNCs on AuNPs to form AuNPs@DNA-AgNCs. On the other hand, p-sulfonated calix[4]arene (pSC4) modified Au is chosen to immobilize the secondary antibody (anti-AFP antibody 2, Ab2) through host-guest recognition between Ab2 and pSC4. When AFP is encountered, the immunoreaction signal can be significantly amplified by the electrochemical reduction of AgNCs. Under optimal circumstances, the sandwich-type electrochemical immunosensor exhibits broad limit of linearity from 0.001 to 100 ng mL-1 (R2 = 0.997) and low detection limit of 7.74 fg mL-1 (S/N = 3). The immunosensor possesses excellent repeatability and selectivity, offering a novel method for sensitive clinical diagnosis of tumor markers in human hepatocellular carcinoma.

An ultrasensitive immunosensor based on cellulose nanofibrils/polydopamine/Cu-Ag nanocomposite for the detection of AFP.

In this work, an ultrasensitive immunosensor for amperometric determination of alpha-fetoprotein (AFP) was developed utilizing Ag and Cu nanoparticles on polydopamine (PDA) functionalized cellulose nanofibrils (CNFs) composite (CNFs/PDA/Cu-Ag) as signal amplifier. PDA was first prepared by self-polymerizing of dopamine, and then was adsorbed on CNFs. The obtained CNFs/PDA was applied as substrate to electrolessly deposit Cu-Ag nanoparticles, using NaBH4 as reducing agent. The structure and morphology of the synthesized CNFs/PDA/Cu-Ag nanocomposite were analyzed through Fourier transform infrared spectroscopy, X-ray photoelectron spectroscopy, X-ray powder diffraction, scanning electron microscopy, particle size analyzer and transmission electron microscopy. The CNFs/PDA/Cu-Ag modified glassy carbon electrode can fix AFP antibody (Ab), and further capture AFP specifically. Electrochemical impedance spectroscopy and cyclic voltammetry were used to characterize the assembly process of immunosensor. The immunoreaction was amplified by electrocatalytical reduction of H2O2 on Cu-Ag nanoparticles, through which AFP was quantitatively detected. The developed sensor exhibits wide linear range of 0.01-100 ng mL-1 (R2 = 0.9963) with low detection limit of 4.27 pg mL-1 (S/N = 3). In addition, it has been used for the detection of AFP in human serum, manifesting its preeminent application prospect in early liver cancer diagnosis.

Emodin alleviates sepsis-mediated lung injury via inhibition and reduction of NF-kB and HMGB1 pathways mediated by SIRT1.

Inflammation plays an important role during sepsis, and excessive inflammation can result in organ damage, chronic inflammation, fibrosis, and scarring. The study aimed to investigate the specific mechanism of emodin by constructing in vivo and in vitro septic lung injury models via inhibition and reduction of NF-kB and high mobility group box 1 (HMGB1) pathways. A cecal ligation and puncture (CLP) model was built for adult male Sprague-Dawley rats. Concentrations of TNF-α, IL-1ß, and IL-6 in bronchoalveolar lavage fluid were determined using commercially available ELISA kits. Hematoxylin and eosin staining was used for the right lung inferior lobes. Myeloperoxidase (MPO) activity of the lung tissue was detected by using the MPO kit. Murine alveolar epithelial cell line (MLE-12) cells were used for flow cytometry and Western blot to analyze the apoptosis rate and protein expression. Emodin significantly decreased CLP-induced cell apoptosis, upregulated expression of sirtuin 1 (SIRT1), and inhibited p-p65/p65 and HMGB1. In lipopolysaccharide (LPS) treated cell model, emodin treatment markedly decreased LPS-induced release of IL-1, IL-6, and tumor necrosis factor (TNF)-α, inhibited LPS-induced cell apoptosis and suppressed protein levels of P-P65/P65 and HMGB1. However, science of SIRT1 reversed the above effects by treatment of emodin. In summarize, this study found that emodin can alleviate sepsis-induced lung injury in vivo and in vitro through regulation of SIRT1.