Combined physical confinement and chemical adsorption on co-doped hollow TiO2 for long-term cycle lithium-sulfur batteries.

Lithium-sulfur (Li-S) batteries have long been expected to be promising high-energy-density secondary batteries because of their high theoretical specific capacity and element abundances. Yet, their poor cyclability and low rate-capacity strongly limited their practical application. Herein, a nitrogen and sulfur dual doped hollow TiO2 sphere is designed and synthesized for the sulfur host. The dual doped hollow TiO2 can enhance the adsorption ability of soluble lithium polysulfides, which effectively promote the conversion reaction of lithium polysulfides from high-order to low-order in Li-S batteries. What is more, the hollow spherical TiO2 host provides a deposition space for lithium polysulfides and blocks polysulfide migration from the cathode to the electrolyte. Both theoretical calculations and experimental studies confirmed that the electrochemical properties of the sulfur electrode are significantly improved by the dual doped hollow TiO2 sphere. The typical as-prepared dual doped hollow TiO2 cathode coated sulfur has a capacity of 1258 mA h g-1 for the first discharge and a capacity decay as low as 0.0648% per cycle during 500 cycles with a sulfur loading of 3.8 mg cm-2.

APE1/Ref-1 prevents oxidative inactivation of ERK for G1-to-S progression following lead acetate exposure.

Apurinic/apyrimidinic endonuclease 1 (APE1)/redox effector factor-1 is a multifunctional enzyme involved in DNA base excision repair and protein redox regulation. Previously, we have showed that lead acetate (Pb) elicits EGFR activation to initiate the SFK/PKCα/Ras/Raf-1/MKK1/2/ERK signaling cascade functioning against genotoxicity. Here, we explore whether APE1 and reactive oxygen species (ROS) affect ERK signaling and cell cycle progression following Pb exposure. We found that Pb induced APE1 expression and ROS generation in CL3 human lung cancer cells. The Pb-elicited ROS levels and cytotoxicity were further enhanced by introducing small interfering RNA specific for APE1 (siAPE1). E3330, an inhibitor of APE1 redox activity, also augmented the ROS levels and cytotoxicity in Pb-treated cells. Intriguingly, the capability of Pb to activate ERK was abolished under siAPE1 or E3330 co-treatments; conversely, forced expression of APE1 up-regulated the ERK activation by Pb or serum in both Cys65-redox activity dependent and independent manners. Moreover, APE1 formed complex with ERK2, and its redox activity could rescue ERK oxidative inactivation. APE1 redox activity also facilitated the Cyclin D1 expression and G1-to-S progression following Pb exposure. In summary, the results indicate that APE1 is a direct redox regulator of ERK for maintaining the kinase activity to promote cell proliferation.

Effects of (-)-epigallocatechin gallate on RPE cell migration and adhesion.

PURPOSE: In diseases such as proliferative vitreoretinopathy (PVR), proliferative diabetic retinopathy (PDR), and age-related macular degeneration (AMD), retinal pigment epithelial (RPE) cells can initiate proliferation and migration and secrete extracellular matrix (ECM) proteins. (-)-Epigallocatechin gallate (EGCG)-a natural anti-oxidant flavonoid that is abundant in green tea-has been shown to suppress the migration and adhesion of many cell types, but its effects on RPE cell migration and adhesion were unknown. Several studies have shown that platelet-derived growth factor (PDGF) enhances proliferation and migration effects on RPE cells in PVR, and that fibronectin is a major ECM component of PVR tissue. Therefore, we investigated the inhibitory effects of EGCG on RPE cell migration induced by PDGF-BB, an isoform of PDGF, and adhesion by fibronectin. METHODS: The migration of RPE cells was detected by an electric cell-substrate impedance sensing (ECIS) migration assay and a Transwell migration assay. Cells were loaded with 2',7'-bis-(carboxyethyl)-5(6')-carboxyfluorescein acetoxymethyl ester (BCECF/AM), and their adhesion to fibronectin was examined. The interactions of EGCG with PDGF-BB were analyzed by a dot binding assay. Cytoskeletal reorganization was examined by immunofluorescence microscopy. The PDGF-BB-induced signaling pathways were detected by western blotting. RESULTS: In the present study, we find that EGCG can inhibit PDGF-BB-induced human RPE cell migration and, in a dose-dependent manner, RPE cell adhesion to fibronectin. Our analysis demonstrates that EGCG does not directly bind to PDGF-BB and the inhibition of EGCG against fibronectin-induced cytoskeletal reorganization is observed. Furthermore, EGCG is shown to suppress PDGF-BB-induced PDGF-beta receptors, downstream PI3K/Akt, and MAPK phosphorylation. CONCLUSIONS: Our results provide the first evidence that EGCG is an effective inhibitor of RPE cell migration and adhesion to fibronectin and, therefore, may prevent epiretinal membrane formation.

Protective effects of (-)-epigallocatechin gallate on UVA-induced damage in ARPE19 cells.

PURPOSE: Oxidative injury to the retinal pigment epithelium (RPE) has been proposed to play a contributing role in age-related macular degeneration (AMD). Exposure to solar ultraviolet (UV) radiation is believed to cause the production of reactive oxygen species (ROS), which may cause oxidative damage to RPE cells. Studies have shown that (-)-epigallocatechin gallate (EGCG), an abundant and active component in green tea, can protect several cell types from oxidative stress. It may be useful in the prevention of early AMD. METHODS: To determine whether EGCG protects RPE cells from UVA-induced damage, we used a cell viability assay to determine the viability of UVA-treated cells. Intracellular H(2)O(2) levels were measured by flow cytometry. Western blotting was used to detect UVA-induced signaling pathways. RESULTS: The results indicated that EGCG inhibits UVA-induced RPE cell death. In addition, intracellular H(2)O(2) generation in RPE cells irradiated by UVA was inhibited by EGCG in a concentration-dependent manner. EGCG also inhibited UVA-induced extracullar signal-regulated kinase (ERK) and c-jun-NH2 terminal kinase (JNK) activation in RPE cells while a higher concentration of EGCG had an inhibitory effect on UVA-induced p38 activation. Finally, we investigated cyclooxygenase-2 (COX-2) expression in RPE cells exposed to UVA radiation, and EGCG was found to also have inhibited UVA-induced COX-2 expression. CONCLUSIONS: Taken together, our results demonstrate that EGCG inhibits UVA-induced H(2)O(2) production, mitogen-activating protein kinase activation, and expression of COX-2. Moreover, it enhances RPE cell survival after UVA exposure. This suggests EGCG is effective in preventing UVA-induced damage in RPE cells and may be suitable for further developments as a chemoprotective factor for the primary prevention of early AMD.