RESUMO
Tungsten disulfide (WS2) nanosheets supported poly(xanthurenic acid) (PXa) was used as the signal transduction interface for electrochemical genosensing. The WS2 nanosheets were obtained from bulk WS2 using a simple ultrasonic method. Due to the unique physical adsorption of Xa monomers to WS2, the electropolymerization efficiency was greatly improved, accompanied with an increased electrochemical response of PXa. The obtained PXa/WS2 nanocomposite not only served as a substrate for DNA immobilization but also reflected the electrochemical transduction originating from DNA immobilization and hybridization without any other indicators or complicated labelling steps. Owing to the presence of abundant carboxyl groups, the probe ssDNA was covalently attached on the carboxyl-terminated PXa/WS2 nanocomposite through the free amines of DNA sequences based on the 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide and N-hydrosulfosuccinimide crosslinking reaction. The covalently immobilized probe ssDNA could selectively hybridize with its target DNA to form dsDNA on the surface of the PXa/WS2 nanocomposite. This developed biosensor achieved a satisfactory detection limit down to 1.6 × 10-16 mol L-1 and a dynamic range of 1.0 × 10-15 to 1.0 × 10-11 mol L-1 for detection of circulating tumor DNA related to gastric carcinoma. Selectivity of the biosensor has been investigated in presence of non-complementary, one-mismatched and two-mismatched DNA sequences.
RESUMO
BACKGROUND: With the rise of the burden of ischemic heart disease, both clinical and economic evidence show a desperate need to protect the heart against myocardium ischemia-reperfusion injury-related complications following cardiac surgery or percutaneous coronary intervention. However, there is no effective intervention for myocardium ischemia-reperfusion injury as yet. METHODS: We pretreated mice with 4 daily 2.0 absolute atmosphere (ATA) hyperbaric oxygen, then observed its effects on heart function parameters and infarct size following in situ ischemia-reperfusion. Multiple oxidative and inflammation products were measured in the myocardium. Next, we investigated the expression of heme oxygenase 1 (HO-1), phosphatidylinositol 3-kinase (PI3K)/serine/threonine protein kinase (Akt) pathway, and NF-E2-related factor 2 (Nrf2) in the presence of myocardium ischemia-reperfusion injury, hyperbaric oxygen preconditioning, and their inhibitors and their effects on heart function parameters. RESULTS: Hyperbaric oxygen preconditioning ameliorated the cardiac function and histological alterations induced by myocardium ischemia-reperfusion injury, decreased oxidative products and proinflammatory cytokine. Hyperbaric oxygen preconditioning increased expression of HO-1, which was suppressed by PI3K inhibitor LY294002, Nrf2 knockout, and Akt inhibitor triciribine. The expression of Nrf2 was enhanced by hyperbaric oxygen preconditioning, but decreased by LY294002 and triciribine. The Akt was also activated by hyperbaric oxygen preconditioning but suppressed by LY294002. The hemodynamic assays showed that cardiac function was suppressed by LY294002, Nrf2 knockout, and triciribine. CONCLUSION: These data present a novel signaling mechanism by which hyperbaric oxygen preconditioning protects myocardium ischemia-reperfusion injury via PI3K/Akt/Nrf2-dependent antioxidant defensive system.