Metal-Free Carbon Quantum Dots Implant Graphitic Carbon Nitride: Enhanced Photocatalytic Dye Wastewater Purification with Simultaneous Hydrogen Production.

The use of photocatalysts to purify wastewater and simultaneously convert solar energy into clean hydrogen energy is of considerable significance in environmental science. However, it is still a challenge due to their relatively high costs, low efficiencies, and poor stabilities. In this study, a metal-free carbon quantum dots (CQDs) modified graphitic carbon nitride photocatalyst (CCN) was synthesized by a facile method. The characterization and theoretical calculation results reveal that the incorporation of CQDs into the g-C3N4 matrix significantly improves the charge transfer and separation efficiency, exhibits a redshift of absorption edge, narrows the bandgap, and prevents the recombination of photoexcited carriers. The hydrogen production and simultaneous degradation of methylene blue (MB) or rhodamine B (RhB) in simulated wastewaters were further tested. In the simulated wastewater, the CCN catalyst showed enhanced photodegradation efficiency, accompanied with the increased hydrogen evolution rate (1291 µmol·h-1·g-1). The internal electrical field between the g-C3N4 and the CQDs is the main reason for the spatial separation of photoexcited electron-hole pairs. Overall, this work could offer a new protocol for the design of highly efficient photocatalysts for dye wastewater purification with simultaneous hydrogen production.

Sinomenine alleviates high glucose-induced renal glomerular endothelial hyperpermeability by inhibiting the activation of RhoA/ROCK signaling pathway.

As an early sign of diabetic cardiovascular disease, endothelial dysfunction may contribute to progressive diabetic nephropathy (DN). Endothelial hyperpermeability induced by hyperglycemia (HG) is a central pathogenesis for DN. Sinomenine (SIN) has strong anti-inflammatory and renal protective effects, following an unknown protective mechanism against HG-induced hyperpermeability. We herein explored the role of SIN in vitro in an HG-induced barrier dysfunction model in human renal glomerular endothelial cells (HRGECs). The cells were exposed to SIN and/or HG for 24 h, the permeability of which was significantly increased by HG. Moreover, junction protein occludin in the cell-cell junction area and its total expression in HRGECs were significantly decreased by HG. However, the dysfunction of tight junction and hyperpermeability of HRGECs were significantly reversed by SIN. Furthermore, SIN prevented HG-increased reactive oxygen species (ROS) by activating nuclear factor-E2-related factor 2 (Nrf2). Interestingly, activation of RhoA/ROCK induced by HG was reversed by SIN or ROCK inhibitor. HG-induced hyperpermeability was prevented by SIN. High ROS level, tight junction dysfunction and RhoA/ROCK activation were significantly attenuated with knockdown of Nrf2. Mediated by activation of Nrf2, SIN managed to significantly prevent HG-disrupted renal endothelial barrier function by suppressing the RhoA/ROCK signaling pathway through reducing ROS. We successfully identified a novel pathway via which SIN exerted antioxidative and renal protective functions, and provided a molecular basis for potential SIN applications in treating DN vascular disorders.