ABSTRACT
The electrochemical CO2 reduction reaction (CO2RR) provides an alternative protocol to producing industrial chemicals with renewable electricity sources, and the highly selective, durable, and economic catalysts should expedite CO2RR applications. Here, we demonstrate a composite Cu-In2O3 catalyst in which a trace amount of In2O3 decorated on Cu surface greatly improves the selectivity and stability for CO2-to-CO reduction as compared to the counterparts (Cu or In2O3), realizing a CO faradaic efficiency (FECO) of 95% at -0.7 V (vs RHE) and no obvious degradation within 7 h. In situ X-ray absorption spectroscopy reveals that In2O3 undergoes the redox reaction and preserves the metallic state of Cu during the CO2RR process. Strong electronic interaction and coupling occur at the Cu/In2O3 interface which serves as the active site for selective CO2RR. Theoretical calculation confirms the roles of In2O3 in preventing oxidation and altering the electronic structure of Cu to assist COOH* formation and demote CO* adsorption at the Cu/In2O3 interface.
ABSTRACT
Platycodon D (PD) and D3 (PD3) isolated from Platycodon grandiflorum has been previously reported to show anti-inflammatory activities in rats. In this study, the production of proinflammatory cytokines, nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) was examined in a macrophage like cell line, RAW 264.7 cells, in the presence of PD and PD3, oligosaccharide derivatives of oleanolic acid. RAW 264.7 cells activated with lipopolysaccharide (LPS; 1 microg/ml) and recombinant interferon-gamma (rIFN-gamma; 50 U/ml) were treated with various doses of PD and PD3 for 24 h. Supernatants were analyzed for the production of NO and TNF-alpha using Griess reagent and enzyme-linked immunosorbent assay (ELISA), respectively. NO was inhibited in a dose-dependent manner by PD and PD3 (IC50 of platycodin D approximately 15 uM, IC50 PD3 approximately 55 uM). The expression of inducible NOS (iNOS) was inhibited by these compounds, as measured by Western blot analysis, as well as the expression of iNOS mRNA, as measured by Northern blot analysis. RAW 264.7 cells were treated at various times after LPS and activation with PD. Treatment with PD up to 8 h after activation showed significant inhibition of NO, indicating that early signal transduction of NOS synthesis may be inhibited by PD. In contrast to NO, secretion of TNF-alpha as well as expression of TNF-alpha mRNA was increased by PD and PD3. TNF-alpha secretion from RAW 264.7 cells was measured at various times after LPS and rIFN-gamma activation. Secretion of TNF-alpha was also increased up to 8 h postactivation, suggesting that PD may stimulate TNF-alpha synthesis or inhibit degradation of TNF-alpha mRNA. Oleanolic acid was without effect on both the production of NO and secretion of TNF-alpha. These data suggest a dichotomous regulation of these important proinflammatory mediators by PD and PD3.