A novel electrochemical horseradish peroxidase (HRP) sensor was developed based on boronate affinity-based electropolymerized polythionine (PTh) molecularly imprinted polymer (MIP) as specific recognition element for HRP on gold nanoparticles (AuNPs) modified glassy carbon electrode, in which PTh acted as the electrochemical probe for the sensor. The sensor was characterized by scanning electron microscopy and electron dispersive spectroscopy. Electrochemical impedance spectroscopy, cyclic voltammetry, and differential pulse voltammetry were exploited for the study of the properties of the MIP sensor. The MIP sensor exhibited excellent linear response over the range of 2.0 × 10−10 mg/mL ∼ 1.0 × 10−7 mg/mL for HRP. In addition, with MIP film as HRP immobilized matrices, the sensor for the detection of H2O2 was developed with the MIP sensor based on the reduction of H2O2 catalyzed by HRP in the presence of electron mediator PTh. The sensor showed linear relationships between the current response and H2O2 concentration from 6.0 × 10−7 to 2.0 × 10−5 mol/L. HRP and H2O2 bi-analyte sensor based on MIP film was successfully developed in this work. The developed method can also be applicable for enzyme and its enzymatic substrate bi-analyte sensor.
Exogenous polysulfhydryls (R-SH) supplementation and nitric oxide (NO) gas molecules delivery provide essential antioxidant buffering pool components and anti-inflammatory species in cellular defense against injury, respectively. Herein, the intermolecular disulfide bonds in bovine serum albumin (BSA) molecules were reductively cleaved under native and mild conditions to expose multiple sulfhydryl groups (BSA-SH), then sulfhydryl-nitrosylated (R-SNO), and nanoprecipitated to form injectable self-sulfhydrated, nitro-fixed albumin nanoparticles (BSA-SNO NPs), allowing albumin to act as a NO donor reservoir and multiple sulfhydryl group transporter while also preventing unfavorable oxidation and self-cross-linking of polysulfhydryl groups. In two mouse models of ischemia/reperfusion-induced and endotoxin-induced acute liver injury (ALI), a single low dosage of BSA-SNO NPs (S-nitrosothiols: 4 μmol·kg–1) effectively attenuated oxidative stress and systemic inflammation cascades in the upstream pathophysiology of disease progression, thus rescuing dying hepatocytes, regulating host defense, repairing microcirculation, and restoring liver function. By mechanistically upregulating the antioxidative signaling pathway (Nrf-2/HO-1/NOQ1) and inhibiting the inflammatory cytokine storm (NF-κB/p-IκBα/TNF-α/IL-β), BSA-SNO NPs blocked the initiation of the mitochondrial apoptotic signaling pathway (Cyto C/Bcl-2 family/caspase-3) and downregulated the cell pyroptosis pathway (NLRP3/ASC/IL-1β), resulting in an increased survival rate from 26.7 to 73.3%. This self-sulfhydrated, nitro-fixed functionalized BSA nanoformulation proposes a potential drug-free treatment strategy for ALI.
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